% % This file was created by the TYPO3 extension % publications % --- Timezone: CEST % Creation date: 2022-12-02 % Creation time: 14:42:44 % --- Number of references % 283 % @Article { Loft2022, author = {Loft, Anne and Schmidt, S{\o}ren Fisker and Caratti, Giorgio and Stifel, Ulrich and Havelund, Jesper and Sekar, Revathi and Kwon, Yun and Sulaj, Alba and Chow, Kan Kau and Alfaro, Ana Jimena and Schwarzmayr, Thomas and Rittig, Nikolaj and Svart, Mads and Tsokanos, Foivos-Filippos and Maida, Adriano and Blutke, Andreas and Feuchtinger, Annette and M{\o}ller, Niels and Bl{\"u}her, Matthias and Nawroth, Peter and Szendr{\"o}di, Julia and F{\ae}rgeman, Nils J. and Zeigerer, Anja and Tuckermann, Jan and Herzig, Stephan}, title = {A macrophage-hepatocyte glucocorticoid receptor axis coordinates fasting ketogenesis.}, abstract = {Fasting metabolism and immunity are tightly linked; however, it is largely unknown how immune cells contribute to metabolic homeostasis during fasting in healthy subjects. Here, we combined cell-type-resolved genomics and computational approaches to map crosstalk between hepatocytes and liver macrophages during fasting. We identified the glucocorticoid receptor (GR) as a key driver of fasting-induced reprogramming of the macrophage secretome including fasting-suppressed cytokines and showed that lack of macrophage GR impaired induction of ketogenesis during fasting as well as endotoxemia. Mechanistically, macrophage GR suppressed the expression of tumor necrosis factor (TNF) and promoted nuclear translocation of hepatocyte GR to activate a fat oxidation/ketogenesis-related gene program, cooperatively induced by GR and peroxisome proliferator-activated receptor alpha (PPARα) in hepatocytes. Together, our results demonstrate how resident liver macrophages directly influence ketogenesis in hepatocytes, thereby also outlining a strategy by which the immune system can set the metabolic tone during inflammatory disease and infection.}, year = {2022}, month = {Mar}, language = {eng}, journal = {Cell metabolism}, volume = {34}, address = {United States}, pages = {473-486.e9}, keywords = {fasting, genomics, glucocorticoid receptor, hepatocyte, ketogenesis, liver, macrophage, nuclear receptor, transcripional regulation, tumor necrosis factor} } @Article { Krueger2022, author = {Kr{\"u}ger, Benjamin Thilo and Steppe, Lena and Vettorazzi, Sabine and Haffner-Luntzer, Melanie and Lee, Sooyeon and Dorn, Ann-Kristin and Ignatius, Anita and Tuckermann, Jan and Ahmad, Mubashir}, title = {Inhibition of Cdk5 Ameliorates Skeletal Bone Loss in Glucocorticoid-Treated Mice.}, abstract = {Glucocorticoids (GCs) are widely used to treat inflammatory diseases. However, their long-term use leads to glucocorticoid-induced osteoporosis, increasing morbidity and mortality. Both anabolic and anti-resorptive drugs are used to counteract GC-induced bone loss, however, they are expensive and/or have major side effects. Therefore, identifying new targets for cost-effective, small-molecule inhibitors is essential. We recently identified cyclin-dependent kinase 5 (Cdk5) as a suppressor of osteoblast differentiation and showed that its inhibition with roscovitine promoted osteoblastogenesis, thus improving the skeletal bone mass and fracture healing. Here, we assessed whether Cdk5 knockdown or inhibition could also reverse the GC-mediated suppression of osteoblast differentiation, bone loss, and fracture healing. We first demonstrated that Cdk5 silencing abolished the dexamethasone (Dex)-induced downregulation of alkaline phosphatase (Alp) activity, osteoblast-specific marker gene expression (Runx2, Sp7, Alpl, and Bglap), and mineralization. Similarly, Cdk5 inhibition rescued Dex-induced suppression of Alp activity. We further demonstrated that Cdk5 inhibition reversed prednisolone (Pred)-induced bone loss in mice, due to reduced osteoclastogenesis rather than improved osteoblastogenesis. Moreover, we revealed that Cdk5 inhibition failed to improve Pred-mediated impaired fracture healing. Taken together, we demonstrated that Cdk5 inhibition with roscovitine ameliorated GC-mediated bone loss but did not reverse GC-induced compromised fracture healing in mice.}, year = {2022}, month = {Feb}, language = {eng}, journal = {Biomedicines}, volume = {10}, address = {Switzerland}, keywords = {bone, cyclin-dependent kinase 5, fracture healing, glucocorticoid-induced osteoporosis, glucocorticoids, osteoblasts, osteoclasts, osteocytes, roscovitine} } @Article { Caratti2022, author = {Caratti, Bozhena and Fidan, Miray and Caratti, Giorgio and Breitenecker, Kristina and Engler, Melanie and Kazemitash, Naser and Traut, Rebecca and Wittig, Rainer and Casanova, Emilio and Ahmadian, Mohammad Reza and Tuckermann, Jan P. and Moll, Herwig P. and Cirstea, Ion Cristian}, title = {The glucocorticoid receptor associates with RAS complexes to inhibit cell proliferation and tumor growth.}, abstract = {Mutations that activate members of the RAS family of GTPases are associated with various cancers and drive tumor growth. The glucocorticoid receptor (GR), a member of the nuclear receptor family, has been proposed to interact with and inhibit the activation of components of the PI3K-AKT and MAPK pathways downstream of RAS. In the absence of activating ligands, we found that GR was present in cytoplasmic KRAS-containing complexes and inhibited the activation of wild-type and oncogenic KRAS in mouse embryonic fibroblasts and human lung cancer A549 cells. The DNA binding domain of GR was involved in the interaction with KRAS, but GR-dependent inhibition of RAS activation did not depend on the nuclear translocation of GR. The addition of ligand released GR-dependent inhibition of RAS, AKT, the MAPK p38, and the MAPKK MEK. CRISPR-Cas9-mediated deletion of GR in A549 cells enhanced tumor growth in xenografts in mice. Patient samples of non-small cell lung carcinomas showed lower expression of , the gene encoding GR, compared to adjacent normal tissues and lower expression correlated with a worse disease outcome. These results suggest that glucocorticoids prevent the ability of GR to limit tumor growth by inhibiting RAS activation, which has potential implications for the use of glucocorticoids in patients with cancer.}, year = {2022}, month = {mar}, issn = {1937-9145}, DOI = {10.1126/scisignal.abm4452}, journal = {Science signaling}, volume = {15}, pages = {eabm4452}, keywords = {Animals; Cell Proliferation; Fibroblasts, metabolism; Humans; Lung Neoplasms, drug therapy, genetics; Mice; Phosphatidylinositol 3-Kinases, metabolism; Receptors, Glucocorticoid, genetics, metabolism} } @Article { Schoppa2022, author = {Schoppa, Astrid M. and Chen, Xiangxu and Ramge, Jan-Moritz and Vikman, Anna and Fischer, Verena and Haffner-Luntzer, Melanie and Riegger, Jana and Tuckermann, Jan and Scharffetter-Kochanek, Karin and Ignatius, Anita}, title = {Osteoblast lineage Sod2 deficiency leads to an osteoporosis-like phenotype in mice.}, abstract = {Osteoporosis is a systemic metabolic skeletal disease characterized by low bone mass and strength associated with fragility fractures. Oxidative stress, which results from elevated intracellular reactive oxygen species (ROS) and arises in the aging organism, is considered one of the critical factors contributing to osteoporosis. Mitochondrial (mt)ROS, as the superoxide anion (O2-) generated during mitochondrial respiration, are eliminated in the young organism by antioxidant defense mechanisms, including superoxide dismutase 2 (SOD2), the expression and activity of which are decreased in aging mesenchymal progenitor cells, accompanied by increased mtROS production. Using a mouse model of osteoblast lineage cells with Sod2 deficiency, we observed significant bone loss in trabecular and cortical bones accompanied by decreased osteoblast activity, increased adipocyte accumulation in the bone marrow and augmented osteoclast activity, suggestive of altered mesenchymal progenitor cell differentiation and osteoclastogenesis. Furthermore, osteoblast senescence was increased. To date, there are only a few studies suggesting a causal association between mtROS and cellular senescence in tissue in vivo. Targeting SOD2 to improve redox homeostasis could represent a potential therapeutic strategy for maintaining bone health during aging.}, year = {2022}, month = {may}, issn = {1754-8411}, DOI = {10.1242/dmm.049392}, journal = {Disease models {\\&} mechanisms}, volume = {15}, keywords = {Animals; Mice; Osteoblasts, metabolism; Osteoclasts, metabolism; Osteoporosis, metabolism; Phenotype; Reactive Oxygen Species, metabolism; Superoxide Dismutase, metabolism; Mitochondrial dysfunction; Osteoporosis; Reactive oxygen species; Senescence; Skeletal aging} } @Article { Ahmad2022, author = {Ahmad, Mubashir and Kr{\"u}ger, Benjamin Thilo and Kroll, Torsten and Vettorazzi, Sabine and Dorn, Ann-Kristin and Mengele, Florian and Lee, Sooyeon and Nandi, Sayantan and Yilmaz, Dilay and Stolz, Miriam and Tangudu, Naveen Kumar and V{\'a}zquez, David Carro and Pachmayr, Johanna and Cirstea, Ion Cristian and Spasic, Maja Vujic and Ploubidou, Aspasia and Ignatius, Anita and Tuckermann, Jan}, title = {Inhibition of Cdk5 increases osteoblast differentiation and bone mass and improves fracture healing.}, abstract = {Identification of regulators of osteoblastogenesis that can be pharmacologically targeted is a major goal in combating osteoporosis, a common disease of the elderly population. Here, unbiased kinome RNAi screening in primary murine osteoblasts identified cyclin-dependent kinase 5 (Cdk5) as a suppressor of osteoblast differentiation in both murine and human preosteoblastic cells. Cdk5 knockdown by siRNA, genetic deletion using the Cre-loxP system, or inhibition with the small molecule roscovitine enhanced osteoblastogenesis in vitro. Roscovitine treatment significantly enhanced bone mass by increasing osteoblastogenesis and improved fracture healing in mice. Mechanistically, downregulation of Cdk5 expression increased Erk phosphorylation, resulting in enhanced osteoblast-specific gene expression. Notably, simultaneous Cdk5 and Erk depletion abrogated the osteoblastogenesis conferred by Cdk5 depletion alone, suggesting that Cdk5 regulates osteoblast differentiation through MAPK pathway modulation. We conclude that Cdk5 is a potential therapeutic target to treat osteoporosis and improve fracture healing.}, year = {2022}, month = {apr}, issn = {2095-4700}, DOI = {10.1038/s41413-022-00195-z}, journal = {Bone research}, volume = {10}, pages = {33} } @Article { Tschaffon2022, author = {Tschaffon, Miriam E. A. and Reber, Stefan O. and Schoppa, Astrid and Nandi, Sayantan and Cirstea, Ion C. and Aszodi, Attila and Ignatius, Anita and Haffner-Luntzer, Melanie}, title = {A novel in vitro assay to study chondrocyte-to-osteoblast transdifferentiation.}, abstract = {PURPOSE: Endochondral ossification, which involves transdifferentiation of chondrocytes into osteoblasts, is an important process involved in the development and postnatal growth of most vertebrate bones as well as in bone fracture healing. To study the basic molecular mechanisms of this process, a robust and easy-to-use in vitro model is desirable. Therefore, we aimed to develop a standardized in vitro assay for the transdifferentiation of chondrogenic cells towards the osteogenic lineage. METHODS: Murine chondrogenic ATDC5 cells were differentiated into the chondrogenic lineage for seven days and subsequently differentiated towards the osteogenic direction. Gene expression analysis of pluripotency, as well as chondrogenic and osteogenic markers, cell-matrix staining, and immunofluorescent staining, were performed to assess the differentiation. In addition, the effects of Wnt3a and lipopolysaccharides (LPS) on the transdifferentiation were tested by their addition to the osteogenic differentiation medium. RESULTS: Following osteogenic differentiation, chondrogenically pe-differentiated cells displayed the expression of pluripotency and osteogenic marker genes as well as alkaline phosphatase activity and a mineralized matrix. Co-expression of Col2a1 and Col1a1 after one day of osteogenic differentiation indicated that osteogenic cells had differentiated from chondrogenic cells. Wnt3a increased and LPS decreased transdifferentiation towards the osteogenic lineage. CONCLUSION: We successfully established a rapid, standardized in vitro assay for the transdifferentiation of chondrogenic cells into osteogenic cells, which is suitable for testing the effects of different compounds on this cellular process.}, year = {2022}, month = {Jan}, language = {eng}, journal = {Endocrine}, volume = {75}, pages = {266-275}, keywords = {Cartilage to bone transformation, Chondrocyte, Endochondral ossification, Fracture healing, In vitro assay, Transdifferentiation} } @Article { Stifel2022, author = {Stifel, Ulrich and Wolfschmitt, Eva-Maria and Vogt, Josef and Wachter, Ulrich and Vettorazzi, Sabine and Tews, Daniel and Hogg, Melanie and Zink, Fabian and Koll, Nora Maria and Winning, Sandra and Mounier, R{\'e}mi and Chazaud, B{\'e}n{\'e}dicte and Radermacher, Peter and Fischer-Posovszky, Pamela and Caratti, Giorgio and Tuckermann, Jan}, title = {Glucocorticoids coordinate macrophage metabolism through the regulation of the tricarboxylic acid cycle.}, abstract = {OBJECTIVES: Glucocorticoids (GCs) are one of the most widely prescribed anti-inflammatory drugs. By acting through their cognate receptor, the glucocorticoid receptor (GR), GCs downregulate the expression of pro-inflammatory genes and upregulate the expression of anti-inflammatory genes. Metabolic pathways have recently been identified as key parts of both the inflammatory activation and anti-inflammatory polarization of macrophages, immune cells responsible for acute inflammation and tissue repair. It is currently unknown whether GCs control macrophage metabolism, and if so, to what extent metabolic regulation by GCs confers anti-inflammatory activity. METHODS: Using transcriptomic and metabolomic profiling of macrophages, we identified GC-controlled pathways involved in metabolism, especially in mitochondrial function. RESULTS: Metabolic analyses revealed that GCs repress glycolysis in inflammatory myeloid cells and promote tricarboxylic acid (TCA) cycle flux, promoting succinate metabolism and preventing intracellular accumulation of succinate. Inhibition of ATP synthase attenuated GC-induced transcriptional changes, likely through stalling of TCA cycle anaplerosis. We further identified a glycolytic regulatory transcription factor, HIF1α, as regulated by GCs, and as a key regulator of GC responsiveness during inflammatory challenge. CONCLUSIONS: Our findings link metabolism to gene regulation by GCs in macrophages.}, year = {2022}, month = {Mar}, language = {eng}, journal = {Molecular metabolism}, volume = {57}, pages = {101424}, keywords = {*Glucocorticoids, *Immunometabolism, *Macrophage, *Succinate, *TCA Cycle} } @Article { Ahmed2022, author = {Ahmed, Helal Mohammed Mohammed and Nimmagadda, Subbaiah Chary and Al-Matary, Yahya S. and Fiori, Maren and May, Tobias and Frank, Daria and Patnana, Pradeep Kumar and R{\'e}cher, Christian and Schliemann, Christoph and Mikesch, Jan-Henrik and Koenig, Thorsten and Rosenbauer, Frank and Hartmann, Wolfgang and Tuckermann, Jan and D{\"u}hrsen, Ulrich and Lanying, Wei and Dugas, Martin and Opalka, Bertram and Lenz, Georg and Khandanpour, Cyrus}, title = {Dexamethasone-mediated inhibition of Notch signalling blocks the interaction of leukaemia and mesenchymal stromal cells.}, abstract = {Acute myeloid leukaemia (AML) is a haematological malignancy characterized by a poor prognosis. Bone marrow mesenchymal stromal cells (BM MSCs) support leukaemic cells in preventing chemotherapy-induced apoptosis. This encouraged us to investigate leukaemia-BM niche-associated signalling and to identify signalling cascades supporting the interaction of leukaemic cells and BM MSC. Our study demonstrated functional differences between MSCs originating from leukaemic (AML MSCs) and healthy donors (HD MSCs). The direct interaction of leukaemic and AML MSCs was indispensable in influencing AML cell proliferation. We further identified an important role for Notch expression and its activation in AML MSCs contributing to the enhanced proliferation of AML cells. Supporting this observation, overexpression of the intracellular Notch domain (Notch ICN) in AML MSCs enhanced AML cells' proliferation. From a therapeutic point of view, dexamethasone treatment impeded Notch signalling in AML MSCs resulting in reduced AML cell proliferation. Concurrent with our data, Notch inhibitors had only a marginal effect on leukaemic cells alone but strongly influenced Notch signalling in AML MSCs and abrogated their cytoprotective function on AML cells. In vivo, dexamethasone treatment impeded Notch signalling in AML MSCs leading to a reduced number of AML MSCs and improved survival of leukaemic mice. In summary, targeting the interaction of leukaemic cells and AML MSCs using dexamethasone or Notch inhibitors might further improve treatment outcomes in AML patients.}, year = {2022}, month = {Feb}, language = {eng}, journal = {British journal of haematology}, volume = {196}, address = {England}, pages = {995-1006}, keywords = {Animals, Anti-Inflammatory Agents/pharmacology/*therapeutic use, Dexamethasone/pharmacology/*therapeutic use, Humans, Leukemia, Myeloid, Acute/*drug therapy, Male, Mesenchymal Stem Cells/*drug effects, Mice, Receptors, Notch/*drug effects, *acute myeloid leukaemia, *bone marrow microenvironment, *dexamethasone, *mesenchymal stromal cell, *notch} } @Article { Steppe2022, author = {Steppe, Lena and B{\"u}low, Jasmin and Tuckermann, Jan and Ignatius, Anita and Haffner-Luntzer, Melanie}, title = {Correction: Steppe et al. Bone Mass and Osteoblast Activity Are Sex-Dependent in Mice Lacking the Estrogen Receptor α in Chondrocytes and Osteoblast Progenitor Cells. , javax.xml.bind.JAXBElement@5271a512, 2022, , javax.xml.bind.JAXBElement@20d7df5a, , 2902.}, abstract = {The authors would like to make corrections to the reference citations in the original article [...].}, year = {2022}, month = {may}, issn = {1422-0067}, DOI = {10.3390/ijms23116020}, journal = {International journal of molecular sciences}, volume = {23} } @Article { Steppe2022a, author = {Steppe, Lena and B{\"u}low, Jasmin and Tuckermann, Jan and Ignatius, Anita and Haffner-Luntzer, Melanie}, title = {Bone Mass and Osteoblast Activity Are Sex-Dependent in Mice Lacking the Estrogen Receptor α in Chondrocytes and Osteoblast Progenitor Cells.}, abstract = {While estrogen receptor alpha (ERα) is known to be important for bone development and homeostasis, its exact function during osteoblast differentiation remains unclear. Conditional deletion of ERα during specific stages of osteoblast differentiation revealed different bone phenotypes, which were also shown to be sex-dependent. Since hypertrophic chondrocytes can transdifferentiate into osteoblasts and substantially contribute to long-bone development, we aimed to investigate the effects of ERα deletion in both osteoblast and chondrocytes on bone development and structure. Therefore, we generated mice in which the ERα gene was inactivated via a -driven cyclic recombinase (ERα {\\&}amp;nbsp; ). We analyzed the bones of 3-month-old ERα {\\&}amp;nbsp; mice by biomechanical testing, micro-computed tomography, and cellular parameters by histology. Male ERα {\\&}amp;nbsp; mice displayed a significantly increased cortical bone mass and flexural rigidity of the femurs compared to age-matched controls with no active Cre-transgene (ERα ). By contrast, female ERα {\\&}amp;nbsp; mice exhibited significant trabecular bone loss, whereas in cortical bone periosteal and endosteal diameters were reduced. Our results indicate that the ERα in osteoblast progenitors and hypertrophic chondrocytes differentially contributes to bone mass regulation in male and female mice and improves our understanding of ERα signaling in bone cells in vivo.}, year = {2022}, month = {mar}, issn = {1422-0067}, DOI = {10.3390/ijms23052902}, journal = {International journal of molecular sciences}, volume = {23}, keywords = {Animals; Chondrocytes; Estrogen Receptor alpha, genetics; Female; Male; Mice; Mice, Knockout; Osteoblasts; Stem Cells; X-Ray Microtomography; biomechanics; bone; chondrocytes; estrogen; genetic animal model; osteoblasts; receptor knockout; sex steroids} } @Article { Nilsson2022, author = {Nilsson, Karin H. and Wu, Jianyao and Gustafsson, Karin L. and El Shahawy, Maha and Koskela, Antti and Tuukkanen, Juha and Tuckermann, Jan and Henning, Petra and Lerner, Ulf H. and Ohlsson, Claes and Mov{\'e}rare-Skrtic, Sofia}, title = {Estradiol and RSPO3 regulate vertebral trabecular bone mass independent of each other.}, abstract = {Osteoporosis is an age-dependent serious skeletal disease that leads to great suffering for the patient and high social costs, especially as the global population reaches higher age. Decreasing estrogen levels after menopause result in a substantial bone loss and increased fracture risk, whereas estrogen treatment improves bone mass in women. RSPO3, a secreted protein that modulates WNT signaling, increases trabecular bone mass and strength in the vertebrae of mice, and is associated with trabecular density and risk of distal forearm fractures in humans. The aim of the present study was to determine if RSPO3 is involved in the bone-sparing effect of estrogens. We first observed that estradiol (E2) treatment increases RSPO3 expression in bone of ovariectomized (OVX) mice, supporting a possible role of RSPO3 in the bone-sparing effect of estrogens. As RSPO3 is mainly expressed by osteoblasts in the bone, we used a mouse model devoid of osteoblast-derived RSPO3 (Runx2-creRspo3(flox/flox) mice) to determine if RSPO3 is required for the bone-sparing effect of E2 in OVX mice. We confirmed that osteoblast-specific RSPO3 inactivation results in a substantial reduction in trabecular bone mass and strength in the vertebrae. However, E2 increased vertebral trabecular bone mass and strength similarly in mice devoid of osteoblast-derived RSPO3 and control mice. Unexpectedly, osteoblast-derived RSPO3 was needed for the full estrogenic response on cortical bone thickness. In conclusion, although osteoblast-derived RSPO3 is a crucial regulator of vertebral trabecular bone, it is required for a full estrogenic effect on cortical, but not trabecular, bone in OVX mice. Thus, estradiol and RSPO3 regulate vertebral trabecular bone mass independent of each other.NEW {\\&} NOTEWORTHY Osteoblast-derived RSPO3 is known to be a crucial regulator of vertebral trabecular bone. Our new findings show that RSPO3 and estrogen regulate trabecular bone independent of each other, but that RSPO3 is necessary for a complete estrogenic effect on cortical bone.}, year = {2022}, month = {mar}, language = {eng}, journal = {American journal of physiology. Endocrinology and metabolism}, volume = {322}, address = {United States}, pages = {E211-E218}, keywords = {RSPO3, estrogen, trabecular bone} } @Article { 885961345294_2021, author = {Tuckermann, J. and Adams, R. H.}, title = {The endothelium-bone axis in development, homeostasis and bone and joint disease}, year = {2021}, month = {10}, day = {17}, journal = {Nat Rev Rheumatol .}, volume = {17(10)}, pages = {608-620} } @Article { 254086001982_2021, author = {Tschaffon, Miriam E. A. and Reber, S. O. and Schoppa, Astrid and Nandi, S. and Cirstea, I. C. and Aszodi, Attila and Ignatius, A and Haffner-Luntzer, M}, title = {A novel in vitro assay to study chondrocyte-to-osteoblast transdifferentiation}, year = {2021}, month = {9}, day = {16}, journal = {Endocrine} } @Article { 280582275336_2021, author = {Pf{\"a}nder, P. and Burret, U. and Vettorazzi, S. and Eiers, A.-K.}, title = {Deletion of Cdk5 in Macrophages Ameliorates Anti-Inflammatory Response during Endotoxemia through Induction of C-Maf and Il-10}, year = {2021}, month = {9}, day = {6}, journal = {Int J Mol Sci .}, volume = {22(17):9648} } @Article { 169021955614_2021, author = {Nilsson, KH. and Nethander, M. and Koskela, A. and Tuukkanen, J. and Souza, PPC. and Tuckermann, J. and Lerner, U. H. and Mov{\'e}rare-Skrtic, S. and Ohlsson, C. and Richards, J. B. and Zhou, S. and Henning, P. and Shahawy, M. E. and Andersen, T. L. and Ejersted, C. and Wu, J. and Gustafsson, K. L. and Lorentzon, M. and Ruud, L. E. and Tobias, J. H.}, title = {RSPO3 is important for trabecular bone and fracture risk in mice and humans}, year = {2021}, month = {8}, day = {13}, journal = {Nat Commun.}, volume = {12(1)}, pages = {4923} } @Article { 860101497391_2021, author = {Vettorazzi, S. and Tuckermann, J. and Gebhardt, C. and Nalbantoglu, D.}, title = {A guide to changing paradigms of glucocorticoid receptor function-a model system for genome regulation and physiology}, year = {2021}, month = {7}, day = {2}, journal = {The FEBS journal} } @Article { 562171432116_2021, author = {Vuji{\c} Spasi{\c}, M. and Hofbauer, L. C. and Baschant, U. and Rauner, M. and Ledesma-Colunga, M. G. and Weidner, H.}, title = {Shaping the bone through iron and iron-related proteins}, year = {2021}, month = {6}, day = {27}, journal = {Semin Hematol}, volume = {58(3)}, pages = {188-200} } @Article { 508461822902_2021, author = {Vettorazzi, S. and Tuckermann, J. and Cherifi, C and Latourte, A and Casas, J and Cuvillier, O and Richette, P and Ostertag, A and Cohen-Solal, M and Hay, E and Provot, S and Ea, H-K and Ledoux, A}, title = {Inhibition of sphingosine 1-phosphate protects mice against chondrocyte catabolism and osteoarthritis}, year = {2021}, month = {6}, day = {16}, journal = {Osteoarthritis Cartilage}, volume = {29(9)}, pages = {1335-1345} } @Article { 670880642407_2021, author = {Tuckermann, J. and Caratti, G. and Giroud, M. and Tsokanos, FF and Kotschi, S and Khani, S and Jouffe, C and Vogl, E. and Irmler, M. and Glantschnig, C and Gil-Lozano, M and Hass, D and Garcia, MR and Mattijssen, F and Maida, A and Tews, D and Fischer-Posovszky, P and Virtanen, KA and Beckers, J and Wabitsch, M and Uhlenhaut, H and Bl{\"u}her, M and Scheideler, M and Bartelt, A and Herzig, S and Feuchtinger, A and Khan, AA}, title = {HAND2 is a novel obesity-linked adipogenic transcription factor regulated by glucocorticoid signalling}, year = {2021}, month = {5}, day = {20}, journal = {Diabetologia}, volume = {64(8)}, pages = {1850-1865} } @Article { 379824950132_2021, author = {Barnea-Zohar, M. and Winograd-Katz, S. and Reuven, N. and Shalev, M. and Kanaan, M. and Tuckermann, J. and Geiger, B. and Elson, A and Stein, M and Rabie, G and Sekeres, J}, title = {Sorting Nexin 10 as a Key Regulator of Membrane Trafficking in Bone-Resorbing Osteoclasts: Lessons Learned From Osteopetrosis}, year = {2021}, month = {5}, day = {20}, journal = {Front Cell Dev Biol.}, volume = {9:671210} } @Article { 159111526065_2021, author = {Paganoni, R. and Lechel, A. and Vuji{\c} Spasi{\c}, M.}, title = {Iron at the Interface of Hepatocellular Carcinoma}, year = {2021}, month = {04}, day = {15}, journal = {Int. J. Mol. Sci.}, edition = {8}, volume = {22} } @Article { 686870374260_2021, author = {Barnea-Zohar, M. and Winograd-Katz, S. and Shalev, M. and Arman, E. and Reuven, N. and Roth, L. and Golani, O. and Stein, M. and Thalji, F. and Kanaan, M. and Tuckermann, J. and Geiger, B. and Elson, A.}, title = {An SNX10-dependent mechanism down-regulates fusion between mature osteoclasts}, year = {2021}, month = {04}, day = {01}, journal = {J Cell Sci .} } @Article { 262818731092_2021, author = {Lee, S. and Liu, P. and Ahmad, M. and Tuckermann, J. P.}, title = {Leukemia inhibitory factor treatment attenuates the detrimental effects of glucocorticoids on bone in mice}, year = {2021}, month = {04}, journal = {Bone.}, volume = {145}, pages = {115843} } @Article { 946245971438_2021, author = {Engler, M. and Fidan, M. and Nandi, S. and Cirstea, I. C.}, title = {Senescence in RASopathies, a possible novel contributor to a complex pathophenoype}, year = {2021}, month = {03}, journal = {Mech Ageing Dev.}, volume = {194}, pages = {111411} } @Article { 221999574499_2021, author = {Shalev, M. and Arman, E. and Stein, M. and Cohen-Sharir, Y. and Brumfeld, V. and Kapishnikov, S. and Royal, I. and Tuckermann, J. and Elson, A.}, title = {PTPRJ promotes osteoclast maturation and activity by inhibiting Cbl-mediated ubiquitination of NFATc1 in late osteoclastogenesis}, year = {2021}, month = {02}, day = {19}, journal = {FEBS J.} } @Article { 625069318212_2021, author = {Hachemi, Y. and Rapp, A. E. and Dorn, A.-K. and Lee, S. and Kr{\"u}ger, B. T. and Kaiser, K. and Ignatius, A. and Tuckermann, J.}, title = {Intact Glucocorticoid Receptor Dimerization Is Deleterious in Trauma-Induced Impaired Fracture Healing}, year = {2021}, month = {02}, day = {17}, journal = {Front Immunol.}, volume = {11}, pages = {628287} } @Article { 541915629841_2021, author = {Kroon, J. and Schilperoort, M. and In Het Panhuis, W. and van den Berg, R. and van Doeselaar, L. and Verzijl, C. R C and van Trigt, N. and Mol, IM. and Sips, HCM. and van den Heuvel, J. K. and Koorneef, L. L. and van der Sluis, R. J. and Fenzl, A. and Kiefer, F. W. and Vettorazzi, S. and Tuckermann, J. P. and Biermasz, N. R. and Meijer, OC. and Rensen, P. C N and Kooijman, S.}, title = {A physiological glucocorticoid rhythm is an important regulator of brown adipose tissue function}, year = {2021}, month = {02}, day = {03}, journal = {Mol Metab.}, volume = {47}, pages = {101179} } @Article { 906486223077_2021, author = {Najafova, Z. and Liu, P. and Wegwitz, F. and Ahmad, M. and Tamon, L. and Kosinsky, R. L. and Xie, W. and Johnsen, S. A. and Tuckermann, J.}, title = {RNF40 exerts stage-dependent functions in differentiating osteoblasts and is essential for bone cell crosstalk}, year = {2021}, month = {02}, journal = {Cell Death Diff.}, volume = {28}, pages = {700-714}, number = {2} } @Article { Nilsson2021, author = {Nilsson, Karin H. and Henning, Petra and El Shahawy, Maha and Nethander, Maria and Andersen, Thomas Levin and Ejersted, Charlotte and Wu, Jianyao and Gustafsson, Karin L. and Koskela, Antti and Tuukkanen, Juha and Souza, Pedro P. C. and Tuckermann, Jan and Lorentzon, Mattias and Ruud, Linda Engstr{\"o}m and Lehtim{\"a}ki, Terho and Tobias, Jon H. and Zhou, Sirui and Lerner, Ulf H. and Richards, J. Brent and Mov{\'e}rare-Skrtic, Sofia and Ohlsson, Claes}, title = {RSPO3 is important for trabecular bone and fracture risk in mice and humans.}, abstract = {With increasing age of the population, countries across the globe are facing a substantial increase in osteoporotic fractures. Genetic association signals for fractures have been reported at the RSPO3 locus, but the causal gene and the underlying mechanism are unknown. Here we show that the fracture reducing allele at the RSPO3 locus associate with increased RSPO3 expression both at the mRNA and protein levels, increased trabecular bone mineral density and reduced risk mainly of distal forearm fractures in humans. We also demonstrate that RSPO3 is expressed in osteoprogenitor cells and osteoblasts and that osteoblast-derived RSPO3 is the principal source of RSPO3 in bone and an important regulator of vertebral trabecular bone mass and bone strength in adult mice. Mechanistic studies revealed that RSPO3 in a cell-autonomous manner increases osteoblast proliferation and differentiation. In conclusion, RSPO3 regulates vertebral trabecular bone mass and bone strength in mice and fracture risk in humans.}, year = {2021}, month = {aug}, issn = {2041-1723}, DOI = {10.1038/s41467-021-25124-2}, journal = {Nature communications}, volume = {12}, pages = {4923}, keywords = {Animals; Bone Density; Cancellous Bone, injuries, metabolism; Cell Differentiation, genetics; Cell Proliferation, genetics; Cells, Cultured; Fractures, Bone, genetics; Genetic Predisposition to Disease, genetics; Humans; Mendelian Randomization Analysis, methods; Mice, Knockout; Mice, Transgenic; Osteoblasts, cytology, metabolism; Polymorphism, Single Nucleotide; Risk Factors; Thrombospondins, deficiency, genetics} } @Article { 707514503513_2021, author = {Cirstea, Ion C. and Fidan, Miray and Chennappan, S}, title = {Studying Metabolic Abnormalities in the Costello Syndrome HRAS G12V Mouse Model: Isolation of Mouse Embryonic Fibroblasts and Their In Vitro Adipocyte Differentiation}, year = {2021}, journal = {Methods Mol Biol.}, volume = {2262}, pages = {397-409} } @Article { Engler2021, author = {Engler, Melanie and Fidan, Miray and Nandi, Sayantan and Cirstea, Ion Cristian}, title = {Senescence in RASopathies, a possible novel contributor to a complex pathophenoype.}, abstract = {Senescence is a biological process that induces a permanent cell cycle arrest and a specific gene expression program in response to various stressors. Following studies over the last few decades, the concept of senescence has evolved from an antiproliferative mechanism in cancer (oncogene-induced senescence) to a critical component of physiological processes associated with embryonic development, tissue regeneration, ageing and its associated diseases. In somatic cells, oncogenic mutations in RAS-MAPK pathway genes are associated with oncogene-induced senescence and cancer, while germline mutations in the same pathway are linked to a group of monogenic developmental disorders generally termed RASopathies. Here, we consider that in these disorders, senescence induction may result in opposing outcomes, a tumour protective effect and a possible contributor to a premature ageing phenotype identified in Costello syndrome, which belongs to the RASopathy group. In this review, we will highlight the role of senescence in organismal homeostasis and we will describe the current knowledge about senescence in RASopathies. Additionally, we provide a perspective on examples of experimentally characterised RASopathy mutations that, alone or in combination with various stressors, may also trigger an age-dependent chronic senescence, possibly contributing to the age-dependent worsening of RASopathy pathophenotype and the reduction of lifespan.}, year = {2021}, month = {mar}, issn = {1872-6216}, DOI = {10.1016/j.mad.2020.111411}, journal = {Mechanisms of ageing and development}, volume = {194}, pages = {111411}, keywords = {Age Factors; Aging, genetics, metabolism, pathology; Aging, Premature, genetics, metabolism, pathology; Animals; Cell Differentiation; Cell Proliferation; Cellular Senescence; Costello Syndrome, genetics, metabolism, pathology; Ectodermal Dysplasia, genetics, metabolism, pathology; Facies; Failure to Thrive, genetics, metabolism, pathology; Genetic Predisposition to Disease; Heart Defects, Congenital, genetics, metabolism, pathology; Humans; Mitogen-Activated Protein Kinases, metabolism; Mutation; Noonan Syndrome, genetics, metabolism, pathology; Phenotype; Signal Transduction; ras Proteins, genetics, metabolism; Cardio-facio-cutaneous syndrome; Costello syndrome; Germline mutations; Noonan syndrome; Oncogene-induced senescence; Premature ageing; RAS-MAPK; RASopathy; Senescence} } @Article { Elson2021, author = {Elson, Ari and Stein, Merle and Rabie, Grace and Barnea-Zohar, Maayan and Winograd-Katz, Sabina and Reuven, Nina and Shalev, Moran and Sekeres, Juraj and Kanaan, Moien and Tuckermann, Jan and Geiger, Benjamin}, title = {Sorting Nexin 10 as a Key Regulator of Membrane Trafficking in Bone-Resorbing Osteoclasts: Lessons Learned From Osteopetrosis.}, abstract = {Bone homeostasis is a complex, multi-step process, which is based primarily on a tightly orchestrated interplay between bone formation and bone resorption that is executed by osteoblasts and osteoclasts (OCLs), respectively. The essential physiological balance between these cells is maintained and controlled at multiple levels, ranging from regulated gene expression to endocrine signals, yet the underlying cellular and molecular mechanisms are still poorly understood. One approach for deciphering the mechanisms that regulate bone homeostasis is the characterization of relevant pathological states in which this balance is disturbed. In this article we describe one such {\dq}error of nature,{\dq} namely the development of acute recessive osteopetrosis (ARO) in humans that is caused by mutations in sorting nexin 10 (SNX10) that affect OCL functioning. We hypothesize here that, by virtue of its specific roles in vesicular trafficking, SNX10 serves as a key selective regulator of the composition of diverse membrane compartments in OCLs, thereby affecting critical processes in the sequence of events that link the plasma membrane with formation of the ruffled border and with extracellular acidification. As a result, SNX10 determines multiple features of these cells either directly or, as in regulation of cell-cell fusion, indirectly. This hypothesis is further supported by the similarities between the cellular defects observed in OCLs form various models of ARO, induced by mutations in SNX10 and in other genes, which suggest that mutations in the known ARO-associated genes act by disrupting the same plasma membrane-to-ruffled border axis, albeit to different degrees. In this article, we describe the population genetics and spread of the original arginine-to-glutamine mutation at position 51 (R51Q) in SNX10 in the Palestinian community. We further review recent studies, conducted in animal and cellular model systems, that highlight the essential roles of SNX10 in critical membrane functions in OCLs, and discuss possible future research directions that are needed for challenging or substantiating our hypothesis.}, year = {2021}, issn = {2296-634X}, DOI = {10.3389/fcell.2021.671210}, journal = {Frontiers in cell and developmental biology}, volume = {9}, pages = {671210}, keywords = {ARO; SNX10; bone resorption; osteoclast; osteopetrosis; sorting nexin} } @Article { Tuckermann2021, author = {Tuckermann, Jan and Adams, Ralf H.}, title = {The endothelium-bone axis in development, homeostasis and bone and joint disease.}, abstract = {Blood vessels form a versatile transport network that is best known for its critical roles in processes such as tissue oxygenation, metabolism and immune surveillance. The vasculature also provides local, often organ-specific, molecular signals that control the behaviour of other cell types in their vicinity during development, homeostasis and regeneration, and also in disease processes. In the skeletal system, the local vasculature is actively involved in both bone formation and resorption. In addition, blood vessels participate in inflammatory processes and contribute to the pathogenesis of diseases that affect the joints, such as rheumatoid arthritis and osteoarthritis. This Review summarizes the current understanding of the architecture, angiogenic growth and functional properties of the bone vasculature. The effects of ageing and pathological conditions, including arthritis and osteoporosis, are also discussed.}, year = {2021}, month = {oct}, issn = {1759-4804}, DOI = {10.1038/s41584-021-00682-3}, journal = {Nature reviews. Rheumatology}, volume = {17}, pages = {608--620}, keywords = {Aging, physiology; Animals; Arthritis, physiopathology; Bone Development, physiology; Bone Diseases, drug therapy, physiopathology; Bone Regeneration, drug effects, physiology; Bone and Bones, blood supply, physiology, physiopathology; Chondrocytes, physiology; Endothelium, Vascular, physiology, physiopathology; Fractures, Bone, physiopathology; Homeostasis, physiology; Humans; Joint Diseases, drug therapy, physiopathology; Macrophages, physiology; Mice; Neovascularization, Pathologic, drug therapy, physiopathology; Neovascularization, Physiologic, physiology; Osteoblasts, physiology; Osteogenesis, physiology; Osteoporosis, drug therapy, physiopathology; Receptor Cross-Talk, physiology; Synoviocytes, physiology} } @Article { Reichardt2021, author = {Reichardt, Sybille D. and Amouret, Agathe and Muzzi, Chiara and Vettorazzi, Sabine and Tuckermann, Jan P. and L{\"u}hder, Fred and Reichardt, Holger M.}, title = {The Role of Glucocorticoids in Inflammatory Diseases.}, abstract = {For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use.}, year = {2021}, month = {Oct}, language = {eng}, journal = {Cells}, volume = {10}, keywords = {Animals, Disease Models, Animal, Glucocorticoids/*metabolism, Humans, Inflammation/*metabolism/pathology, Models, Biological, Nanoparticles/chemistry, Phenotype, *acute lung injury, *asthma, *glucocorticoid receptor, *graft-versus-host-disease, *inflammatory bowel disease, *multiple sclerosis, *nanoparticles, *rheumatoid arthritis} } @Article { Najafova2021, author = {Najafova, Zeynab and Liu, Peng and Wegwitz, Florian and Ahmad, Mubashir and Tamon, Liezel and Kosinsky, Robyn Laura and Xie, Wanhua and Johnsen, Steven A. and Tuckermann, Jan}, title = {RNF40 exerts stage-dependent functions in differentiating osteoblasts and is essential for bone cell crosstalk.}, abstract = {The role of histone ubiquitination in directing cell lineage specification is only poorly understood. Our previous work indicated a role of the histone 2B ubiquitin ligase RNF40 in controlling osteoblast differentiation in vitro. Here, we demonstrate that RNF40 has a stage-dependent function in controlling osteoblast differentiation in vivo. RNF40 expression is essential for early stages of lineage specification, but is dispensable in mature osteoblasts. Paradoxically, while osteoblast-specific RNF40 deletion led to impaired bone formation, it also resulted in increased bone mass due to impaired bone cell crosstalk. Loss of RNF40 resulted in decreased osteoclast number and function through modulation of RANKL expression in OBs. Mechanistically, we demonstrate that Tnfsf11 (encoding RANKL) is an important target gene of H2B monoubiquitination. These data reveal an important role of RNF40-mediated H2B monoubiquitination in bone formation and remodeling and provide a basis for exploring this pathway for the treatment of conditions such as osteoporosis or cancer-associated osteolysis.}, year = {2021}, month = {feb}, issn = {1476-5403}, DOI = {10.1038/s41418-020-00614-w}, journal = {Cell death and differentiation}, volume = {28}, pages = {700--714}, keywords = {Animals; Cell Differentiation; Histones, metabolism; Male; Mice; Mice, Inbred C57BL; Osteocytes, metabolism; Osteogenesis, physiology; RANK Ligand, genetics, metabolism; Ubiquitin-Protein Ligases, genetics, metabolism; Ubiquitination, physiology} } @Article { Fidan2021, author = {Fidan, Miray and Chennappan, Saravanakkumar and Cirstea, Ion Cristian}, title = {Studying Metabolic Abnormalities in the Costello Syndrome HRAS G12V Mouse Model: Isolation of Mouse Embryonic Fibroblasts and Their In Vitro Adipocyte Differentiation.}, abstract = {Costello syndrome (CS), characterized by a developmental delay and a failure to thrive, is also associated with an impaired lipid and energy metabolism. White adipose tissue is a central sensor of whole-body energy homeostasis, and HRAS hyperactivation may affect adipocyte differentiation and mature adipocyte homeostasis. An extremely useful tool for delineating in vitro intrinsic cellular signaling leading to metabolic alterations during adipogenesis is mouse embryonic fibroblasts, known to differentiate into adipocytes in response to adipogenesis-stimulating factors. Here, we describe in detail the isolation and maintenance of CS HRAS G12V mouse embryonic fibroblasts, their differentiation into adipocytes, and an assessment of adipocyte differentiation.}, year = {2021}, issn = {1940-6029}, DOI = {10.1007/978-1-0716-1190-6_24}, journal = {Methods in molecular biology (Clifton, N.J.)}, volume = {2262}, pages = {397--409}, keywords = {Adipocytes, metabolism, pathology; Adipogenesis; Animals; Cell Differentiation; Costello Syndrome, genetics, metabolism, pathology; Disease Models, Animal; Embryo, Mammalian, metabolism, pathology; Female; Fibroblasts, metabolism, pathology; Homeostasis; In Vitro Techniques; Male; Mice; Mice, Knockout; Mutation; Proto-Oncogene Proteins p21(ras), physiology; Adipocyte; Costello syndrome; Development; Embryonic; Fibroblast; Metabolism; Mouse model; RASopathy} } @Article { Shalev2021, author = {Shalev, Moran and Arman, Esther and Stein, Merle and Cohen-Sharir, Yael and Brumfeld, Vlad and Kapishnikov, Sergey and Royal, Isabelle and Tuckermann, Jan and Elson, Ari}, title = {PTPRJ promotes osteoclast maturation and activity by inhibiting Cbl-mediated ubiquitination of NFATc1 in late osteoclastogenesis.}, abstract = {Bone-resorbing osteoclasts (OCLs) are multinucleated phagocytes, whose central roles in regulating bone formation and homeostasis are critical for normal health and development. OCLs are produced from precursor monocytes in a multistage process that includes initial differentiation, cell-cell fusion, and subsequent functional and morphological maturation; the molecular regulation of osteoclastogenesis is not fully understood. Here, we identify the receptor-type protein tyrosine phosphatase PTPRJ as an essential regulator specifically of OCL maturation. Monocytes from PTPRJ-deficient (JKO) mice differentiate and fuse normally, but their maturation into functional OCLs and their ability to degrade bone are severely inhibited. In agreement, mice lacking PTPRJ throughout their bodies or only in OCLs exhibit increased bone mass due to reduced OCL-mediated bone resorption. We further show that PTPRJ promotes OCL maturation by dephosphorylating the M-CSF receptor (M-CSFR) and Cbl, thus reducing the ubiquitination and degradation of the key osteoclastogenic transcription factor NFATc1. Loss of PTPRJ increases ubiquitination of NFATc1 and reduces its amounts at later stages of osteoclastogenesis, thereby inhibiting OCL maturation. PTPRJ thus fulfills an essential and cell-autonomous role in promoting OCL maturation by balancing between the pro- and anti-osteoclastogenic activities of the M-CSFR and maintaining NFATc1 expression during late osteoclastogenesis.}, year = {2021}, month = {aug}, issn = {1742-4658}, DOI = {10.1111/febs.15778}, journal = {The FEBS journal}, volume = {288}, pages = {4702--4723}, keywords = {Animals; Cells, Cultured; Female; Male; Mice; Mice, Inbred C57BL; Monocytes, cytology, metabolism; NFATC Transcription Factors, metabolism; Osteoclasts, cytology, metabolism; Osteogenesis; Proto-Oncogene Proteins c-cbl, metabolism; Receptor, Macrophage Colony-Stimulating Factor, metabolism; Receptor-Like Protein Tyrosine Phosphatases, Class 3, genetics, metabolism; Ubiquitination; Cbl; DEP-1; PTPRJ; osteoclast; protein tyrosine phosphatase} } @Article { Steppe2021, author = {Steppe, Lena and Kr{\"u}ger, Benjamin Thilo and Tschaffon, Miriam Eva Angelica and Fischer, Verena and Tuckermann, Jan and Ignatius, Anita and Haffner-Luntzer, Melanie}, title = {Estrogen Receptor α Signaling in Osteoblasts is Required for Mechanotransduction in Bone Fracture Healing.}, abstract = {Biomechanical stimulation by whole-body low-magnitude high-frequency vibration (LMHFV) has demonstrated to provoke anabolic effects on bone metabolism in both non-osteoporotic and osteoporotic animals and humans. However, preclinical studies reported that vibration improved fracture healing and bone formation in osteoporotic, ovariectomized (OVX) mice representing an estrogen-deficient hormonal status, but impaired bone regeneration in skeletally healthy non-OVX mice. These effects were abolished in general estrogen receptor α (ERα)-knockout (KO) mice. However, it remains to be elucidated which cell types in the fracture callus are targeted by LMHFV during bone healing. To answer this question, we generated osteoblast lineage-specific ERα-KO mice that were subjected to ovariectomy, femur osteotomy and subsequent vibration. We found that the ERα specifically on osteoblastic lineage cells facilitated the vibration-induced effects on fracture healing, because in osteoblast lineage-specific ERα-KO (ERα(fl/fl; Runx2Cre)) mice the negative effects in non-OVX mice were abolished, whereas the positive effects of vibration in OVX mice were reversed. To gain greater mechanistic insights, the influence of vibration on murine and human osteogenic cells was investigated in vitro by whole genome array analysis and qPCR. The results suggested that particularly canonical WNT and Cox2/PGE(2) signaling is involved in the mechanotransduction of LMHFV under estrogen-deficient conditions. In conclusion, our study demonstrates a critical role of the osteoblast lineage-specific ERα in LMHFV-induced effects on fracture healing and provides further insights into the molecular mechanism behind these effects.}, year = {2021}, language = {eng}, journal = {Frontiers in bioengineering and biotechnology}, volume = {9}, pages = {782355}, keywords = {LMHFV, estrogen receptor signaling, fracture healing, osteoblasts, prostaglandin signaling, whole-body vibration, wnt signaling} } @Article { Kroon2021, author = {Kroon, Jan and Schilperoort, Maaike and In Het Panhuis, Wietse and Berg, Rosa and Doeselaar, Lotte and Verzijl, Cristy R. C. and Trigt, Nikki and Mol, Isabel M. and Sips, Hetty H. C. M. and Heuvel, Jose K. and Koorneef, Lisa L. and Sluis, Ronald J. and Fenzl, Anna and Kiefer, Florian W. and Vettorazzi, Sabine and Tuckermann, Jan P. and Biermasz, Nienke R. and Meijer, Onno C. and Rensen, Patrick C. N. and Kooijman, Sander}, title = {A physiological glucocorticoid rhythm is an important regulator of brown adipose tissue function.}, abstract = {Brown adipose tissue (BAT) displays a strong circadian rhythm in metabolic activity, but it is unclear how this rhythm is regulated. As circulating levels of corticosterone coincide with the rhythm of triglyceride-derived fatty acid (FA) uptake by BAT, we investigated whether corticosterone regulates BAT circadian rhythm. Corticosterone levels were flattened by implanting mice with subcutaneous corticosterone-releasing pellets, resulting in constant circulating corticosterone levels. Flattened corticosterone rhythm caused a complete loss of circadian rhythm in triglyceride-derived fatty acid uptake by BAT. This effect was independent of glucocorticoid receptor expression in (brown) adipocytes and was not caused by deregulation of clock gene expression or overexposure to glucocorticoids, but rather seemed mediated by reduced sympathetic innervation of BAT. In a mouse model of hyperlipidemia and metabolic syndrome, long-term experimental flattening of corticosterone - and thus rhythm in BAT function - resulted in adiposity. This study highlights that a physiological rhythm in glucocorticoids is an important regulator of BAT function and essential for the maintenance of metabolic health.}, year = {2021}, month = {may}, issn = {2212-8778}, DOI = {10.1016/j.molmet.2021.101179}, journal = {Molecular metabolism}, volume = {47}, pages = {101179}, keywords = {Adipocytes, metabolism, pathology; Adipose Tissue, Brown, metabolism, pathology; Adiposity; Animals; Circadian Rhythm, physiology; Corticosterone, metabolism; Fatty Acids, metabolism; Female; Glucocorticoids, metabolism; Lipid Metabolism, physiology; Male; Mice; Mice, Inbred C57BL; Obesity, metabolism; Period Circadian Proteins, genetics, metabolism; Receptors, Glucocorticoid, genetics, metabolism; Transcriptome; Triglycerides, metabolism; Brown adipose tissue; Circadian Rhythm; Corticosterone; Glucocorticoid receptor} } @Article { BarneaZohar2021, author = {Barnea-Zohar, Maayan and Winograd-Katz, Sabina E. and Shalev, Moran and Arman, Esther and Reuven, Nina and Roth, Lee and Golani, Ofra and Stein, Merle and Thalji, Fadi and Kanaan, Moien and Tuckermann, Jan and Geiger, Benjamin and Elson, Ari}, title = {An SNX10-dependent mechanism downregulates fusion between mature osteoclasts.}, abstract = {Homozygosity for the R51Q mutation in sorting nexin 10 (SNX10) inactivates osteoclasts (OCLs) and induces autosomal recessive osteopetrosis in humans and in mice. We show here that the fusion of wild-type murine monocytes to form OCLs is highly regulated, and that its extent is limited by blocking fusion between mature OCLs. In contrast, monocytes from homozygous R51Q SNX10 mice fuse uncontrollably, forming giant dysfunctional OCLs that can become 10- to 100-fold larger than their wild-type counterparts. Furthermore, mutant OCLs display reduced endocytotic activity, suggesting that their deregulated fusion is due to alterations in membrane homeostasis caused by loss of SNX10 function. This is supported by the finding that the R51Q SNX10 protein is unstable and exhibits altered lipid-binding properties, and is consistent with a key role for SNX10 in vesicular trafficking. We propose that OCL size and functionality are regulated by a cell-autonomous SNX10-dependent mechanism that downregulates fusion between mature OCLs. The R51Q mutation abolishes this regulatory activity, leading to excessive fusion, loss of bone resorption capacity and, consequently, to an osteopetrotic phenotype in vivo. This article has an associated First Person interview with the joint first authors of the paper.}, year = {2021}, month = {may}, issn = {1477-9137}, DOI = {10.1242/jcs.254979}, journal = {Journal of cell science}, volume = {134}, keywords = {Animals; Bone Resorption, genetics; Mice; Mutation, genetics; Osteoclasts; Osteopetrosis; Sorting Nexins, genetics; Bone; Cell fusion; Osteoclast; Osteopetrosis; SNX10} } @Article { Vettorazzi2021, author = {Vettorazzi, Sabine and Nalbantoglu, Denis and Gebhardt, J. Christof M. and Tuckermann, Jan}, title = {A guide to changing paradigms of glucocorticoid receptor function-a model system for genome regulation and physiology.}, abstract = {The glucocorticoid receptor (GR) is a bona fide ligand-regulated transcription factor. Cloned in the 80s, the GR has become one of the best-studied and clinically most relevant members of the nuclear receptor superfamily. Cooperative activity of GR with other transcription factors and a plethora of coregulators contribute to the tissue- and context-specific response toward the endogenous and pharmacological glucocorticoids (GCs). Furthermore, nontranscriptional activities in the cytoplasm are emerging as an additional function of GR. Over the past 40 years, the concepts of GR mechanisms of action had been constantly changing. Different methodologies in the pregenomic and genomic era of molecular biological research and recent cutting-edge technology in single-cell and single-molecule analysis are steadily evolving the views, how the GR in particular and transcriptional regulation in general act in physiological and pathological processes. In addition to the development of technologies for GR analysis, the use of model organisms provides insights how the GR in vivo executes GC action in tissue homeostasis, inflammation, and energy metabolism. The model organisms, namely the mouse, but also rats, zebrafish, and recently fruit flies carrying mutations of the GR became a major driving force to analyze the molecular function of GR in disease models. This guide provides an overview of the exciting research and paradigm shifts in the GR field from past to present with a focus on GR transcription factor networks, GR DNA-binding and single-cell analysis, and model systems.}, year = {2021}, month = {jul}, issn = {1742-4658}, DOI = {10.1111/febs.16100}, journal = {The FEBS journal}, keywords = {genomic action; glucocorticoid receptor; nongenomic action; nuclear receptor; single-molecule analysis; transcription factor} } @Article { Lee2021, author = {Lee, Sooyeon and Kr{\"u}ger, Benjamin Thilo and Ignatius, Anita and Tuckermann, Jan}, title = {Distinct Glucocorticoid Receptor Actions in Bone Homeostasis and Bone Diseases.}, abstract = {Glucocorticoids (GCs) are steroid hormones that respond to stress and the circadian rhythm. Pharmacological GCs are widely used to treat autoimmune and chronic inflammatory diseases despite their adverse effects on bone after long-term therapy. GCs regulate bone homeostasis in a cell-type specific manner, affecting osteoblasts, osteoclasts, and osteocytes. Endogenous physiological and exogenous/excessive GCs act via nuclear receptors, mainly via the GC receptor (GR). Endogenous GCs have anabolic effects on bone mass regulation, while excessive or exogenous GCs can cause detrimental effects on bone. GC-induced osteoporosis (GIO) is a common adverse effect after GC therapy, which increases the risk of fractures. Exogenous GC treatment impairs osteoblastogenesis, survival of the osteoblasts/osteocytes and prolongs the longevity of osteoclasts. Under normal physiological conditions, endogenous GCs are regulated by the circadian rhythm and circadian genes display oscillatory rhythmicity in bone cells. However, exogenous GCs treatment disturbs the circadian rhythm. Recent evidence suggests that the disturbed circadian rhythm by continuous exogenous GCs treatment can in itself hamper bone integrity. GC signaling is also important for fracture healing and rheumatoid arthritis, where crosstalk among several cell types including macrophages and stromal cells is indispensable. This review summarizes the complexity of GC actions via GR in bone cells at cellular and molecular levels, including the effect on circadian rhythmicity, and outlines new therapeutic possibilities for the treatment of their adverse effects.}, year = {2021}, language = {eng}, journal = {Frontiers in endocrinology}, volume = {12}, pages = {815386}, keywords = {*glucocorticoid receptor, *osteoblast, *osteoclast, *osteoporosis, *transgenic mice} } @Article { Nairz2021, author = {Nairz, Manfred and Metzendorf, Christoph and Vujic-Spasic, Maja and Mitterstiller, Anna-Maria and Schroll, Andrea and Haschka, David and Hoffmann, Alexander and Von Raffay, Laura and Sparla, Richard and Huck, Christian W. and Talasz, Heribert and Moser, Patrizia L. and Muckenthaler, Martina U. and Weiss, G{\"u}nter}, title = {Cell-specific expression of determines the outcome of Salmonella enterica serovar Typhimurium infection in mice.}, abstract = {Mutations in HFE cause hereditary hemochromatosis type I hallmarked by increased iron absorption, iron accumulation in hepatocytes and iron deficiency in myeloid cells. HFE encodes an MHC-I like molecule, but its function in immune responses to infection remains incompletely understood. Here, we investigated putative roles of Hfe in myeloid cells and hepatocytes, separately, upon infection with Salmonella Typhimurium, an intracellular bacterium with iron-dependent virulence. We found that constitutive and macrophage-specific deletion of Hfe protected infected mice. The propagation of Salmonella in macrophages was reduced due to limited intramacrophage iron availability for bacterial growth and increased expression of the anti-microbial enzyme nitric oxide synthase-2. By contrast, mice with hepatocyte-specific deletion of Hfe succumbed earlier to Salmonella infection because of unrestricted extracellular bacterial replication associated with high iron availability in the serum and impaired expression of essential host defense molecules such as interleukin-6, interferon-γ and nitric oxide synthase-2. Wild-type mice subjected to dietary iron overload phenocopied hepatocyte-specific Hfe deficiency suggesting that increased iron availability in the serum is deleterious in Salmonella infection and underlies impaired host immune responses. Moreover, the macrophage-specific effect is dominant over hepatocyte-specific Hfe-depletion, as Hfe knock-out mice have increased survival despite the higher parenchymal iron load associated with systemic loss of Hfe. We conclude that cell-specific expression of Hfe in hepatocytes and macrophages differentially affects the course of infections with specific pathogens by determining bacterial iron access and the efficacy of anti-microbial immune effector pathways. This may explain the high frequency and evolutionary conservation of human HFE mutations.}, year = {2021}, month = {Dec}, language = {eng}, journal = {Haematologica}, volume = {106}, pages = {3149-3161}, keywords = {Animals, *Hemochromatosis, Hemochromatosis Protein/genetics, Mice, Knockout, *Salmonella Infections/genetics, Salmonella typhimurium/genetics, Serogroup} } @Article { Giroud2021, author = {Giroud, Maude and Tsokanos, Foivos-Filippos and Caratti, Giorgio and Kotschi, Stefan and Khani, Sajjad and Jouffe, C{\'e}line and Vogl, Elena S. and Irmler, Martin and Glantschnig, Christina and Gil-Lozano, Manuel and Hass, Daniela and Khan, Asrar Ali and Garcia, Marcos Rios and Mattijssen, Frits and Maida, Adriano and Tews, Daniel and Fischer-Posovszky, Pamela and Feuchtinger, Annette and Virtanen, Kirsi A. and Beckers, Johannes and Wabitsch, Martin and Uhlenhaut, Henriette and Bl{\"u}her, Matthias and Tuckermann, Jan and Scheideler, Marcel and Bartelt, Alexander and Herzig, Stephan}, title = {HAND2 is a novel obesity-linked adipogenic transcription factor regulated by glucocorticoid signalling.}, abstract = {Adipocytes are critical cornerstones of energy metabolism. While obesity-induced adipocyte dysfunction is associated with insulin resistance and systemic metabolic disturbances, adipogenesis, the formation of new adipocytes and healthy adipose tissue expansion are associated with metabolic benefits. Understanding the molecular mechanisms governing adipogenesis is of great clinical potential to efficiently restore metabolic health in obesity. Here we investigate the role of heart and neural crest derivatives-expressed 2 (HAND2) in adipogenesis. Human white adipose tissue (WAT) was collected from two cross-sectional studies of 318 and 96 individuals. In vitro, for mechanistic experiments we used primary adipocytes from humans and mice as well as human multipotent adipose-derived stem (hMADS) cells. Gene silencing was performed using siRNA or genetic inactivation in primary adipocytes from loxP and or tamoxifen-inducible Cre-ERT2 mouse models with Cre-encoding mRNA or tamoxifen, respectively. Adipogenesis and adipocyte metabolism were measured by Oil Red O staining, quantitative PCR (qPCR), microarray, glucose uptake assay, western blot and lipolysis assay. A combinatorial RNA sequencing (RNAseq) and ChIP qPCR approach was used to identify target genes regulated by HAND2. In vivo, we created a conditional adipocyte Hand2 deletion mouse model using Cre under control of the Adipoq promoter (Hand2 ) and performed a large panel of metabolic tests. We found that HAND2 is an obesity-linked white adipocyte transcription factor regulated by glucocorticoids that was necessary but insufficient for adipocyte differentiation in vitro. In a large cohort of humans, WAT HAND2 expression was correlated to BMI. The HAND2 gene was enriched in white adipocytes compared with brown, induced early in differentiation and responded to dexamethasone (DEX), a typical glucocorticoid receptor (GR, encoded by NR3C1) agonist. Silencing of NR3C1 in hMADS cells or deletion of GR in a transgenic conditional mouse model results in diminished HAND2 expression, establishing that adipocyte HAND2 is regulated by glucocorticoids via GR in vitro and in vivo. Furthermore, we identified gene clusters indirectly regulated by the GR-HAND2 pathway. Interestingly, silencing of HAND2 impaired adipocyte differentiation in hMADS and primary mouse adipocytes. However, a conditional adipocyte Hand2 deletion mouse model using Cre under control of the Adipoq promoter did not mirror these effects on adipose tissue differentiation, indicating that HAND2 was required at stages prior to Adipoq expression. In summary, our study identifies HAND2 as a novel obesity-linked adipocyte transcription factor, highlighting new mechanisms of GR-dependent adipogenesis in humans and mice. Array data have been submitted to the GEO database at NCBI (GSE148699).}, year = {2021}, month = {aug}, issn = {1432-0428}, DOI = {10.1007/s00125-021-05470-y}, journal = {Diabetologia}, volume = {64}, pages = {1850--1865}, keywords = {Adipocytes, metabolism; Adipogenesis, physiology; Adipose Tissue, Brown, metabolism; Adult; Aged; Animals; Basic Helix-Loop-Helix Transcription Factors, genetics; Cross-Sectional Studies; Female; Gene Expression Regulation, physiology; Gene Silencing; Glucocorticoids, pharmacology; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Middle Aged; Obesity, genetics; Real-Time Polymerase Chain Reaction; Signal Transduction; Transcription Factors, genetics; Young Adult; Adipocytes; Dexamethasone; Differentiation; Glucocorticoid receptor; HAND2; Human adipose tissue; Mesenchymal stem cells; Obesity; Transcription factor; hMADS} } @Article { Preuss2021, author = {Preuss, Jonathan M. and Burret, Ute and Gr{\"o}ger, Michael and Kress, Sandra and Scheuerle, Angelika and M{\"o}ller, Peter and Tuckermann, Jan P. and Wepler, Martin and Vettorazzi, Sabine}, title = {Impaired Glucocorticoid Receptor Signaling Aggravates Lung Injury after Hemorrhagic Shock.}, abstract = {We previously showed that attenuated lung injury after hemorrhagic shock (HS) coincided with enhanced levels of the glucocorticoid (GC) receptor (GR) in lung tissue of swine. Here, we investigated the effects of impaired GR signaling on the lung during resuscitated HS using a dysfunctional GR mouse model (GR(dim/dim)). In a mouse intensive care unit, HS led to impaired lung mechanics and aggravated lung inflammation in GR(dim/dim) mice compared to wildtype mice (GR(+/+)). After HS, high levels of the pro-inflammatory and pro-apoptotic transcription factor STAT1/pSTAT1 were found in lung samples from GR(dim/dim) mice. Lungs of GR(dim/dim) mice revealed apoptosis, most likely as consequence of reduced expression of the lung-protective Angpt1 compared to GR(+/+) after HS. RNA-sequencing revealed increased expression of pro-apoptotic and cytokine-signaling associated genes in lung tissue of GR(dim/dim) mice. Furthermore, high levels of pro-inflammatory cytokines and iNOS were found in lungs of GR(dim/dim) mice. Our results indicate impaired repression of STAT1/pSTAT1 due to dysfunctional GR signaling in GR(dim/dim) mice, which leads to increased inflammation and apoptosis in the lungs. These data highlight the crucial role of functional GR signaling to attenuate HS-induced lung damage.}, year = {2021}, month = {Dec}, language = {eng}, journal = {Cells}, volume = {11}, keywords = {*glucocorticoid receptor, *hemorrhagic shock, *homodimer, *resuscitation} } @Article { Cherifi2021, author = {Cherifi, C. and Latourte, A. and Vettorazzi, S. and Tuckermann, J. and Provot, S. and Ea, H.-K. and Ledoux, A. and Casas, J. and Cuvillier, O. and Richette, P. and Ostertag, A. and Hay, E. and Cohen-Solal, M.}, title = {Inhibition of sphingosine 1-phosphate protects mice against chondrocyte catabolism and osteoarthritis.}, abstract = {Cartilage loss observed in osteoarthritis (OA) is prevented when osteoclasts in the subchondral bone are inhibited in mice. Here, we investigated the role of the osteoclast secretome and of the lipid mediator sphingosine 1-phosphate (S1P) in chondrocyte metabolism and OA. We used SphK1 and wild type mice to assess the effect of murine osteoclast secretome in chondrocyte metabolism. Gene and protein expressions of matrix metalloproteinase (Mmp) were quantified in chondrocytes and explants by RT-qPCR and Western blots. SphK1 mice or wild type mice treated with S1P receptor inhibitor JTE013 or anti-S1P neutralizing antibody sphingomab are analyzed by OA score and immunohistochemistry. The osteoclast secretome increased the expression of Mmp3 and Mmp13 in murine chondrocytes and cartilage explants and activated the JNK signaling pathway, which led to matrix degradation. JTE013 reversed the osteoclast-mediated chondrocyte catabolism and protected mice against OA, suggesting that osteoclastic S1P contributes to cartilage damage in OA via S1P/S1P signaling. The activity of sphingosine kinase 1 (SphK1) increased with osteoclast differentiation, and its expression was enhanced in subchondral bone of mice with OA. The expression of Mmp3 and Mmp13 in chondrocytes was low upon stimulation with the secretome of Sphk1-lacking osteoclasts. Cartilage damage was significantly reduced in SphK1 mice, but not the synovial inflammation. Finally, intra-articular administration of sphingomab inhibited the cartilage damage and synovial inflammation. Lack of S1P in myeloid cells and local S1P neutralization alleviates from osteoarthritis in mice. These data identify S1P as a therapeutic target in OA.}, year = {2021}, month = {sep}, issn = {1522-9653}, DOI = {10.1016/j.joca.2021.06.001}, journal = {Osteoarthritis and cartilage}, volume = {29}, pages = {1335--1345}, keywords = {Animals; Chondrocytes, metabolism; Lysophospholipids, antagonists {\\&} inhibitors; Male; Mice; Osteoarthritis, metabolism, prevention {\\&} control; Osteoclasts, metabolism; Secretome, metabolism; Sphingosine, analogs {\\&} derivatives, antagonists {\\&} inhibitors; Bone; Cartilage; Metalloproteinase; Osteoarthritis; Sphingosine 1 phosphate} } @Article { Lee2021a, author = {Lee, Sooyeon and Liu, Peng and Ahmad, Mubashir and Tuckermann, Jan P.}, title = {Leukemia inhibitory factor treatment attenuates the detrimental effects of glucocorticoids on bone in mice.}, abstract = {Glucocorticoids (GCs) are widely used drugs for the treatment of inflammatory and autoimmune diseases. However, a severe side effect induced by long-term GC therapy is osteoporosis. Leukemia inhibitory factor (LIF) - a glycoprotein 130 (gp130) dependent cytokine and member of the interleukin-6 cytokine family - is an activator protein 1 (AP-1) target gene that may be involved in one of the mechanisms underlying GC-induced bone loss. Indeed, we previously reported that the mRNA expression level of LIF was enhanced upon osteogenic differentiation, but was significantly decreased in GC-treated osteoblasts. In this study, we show that in vitro LIF treatment rescues the decreased early osteogenic differentiation and mineralization of GC-treated osteoblasts. Furthermore, we also demonstrate that in vivo LIF treatment protects against GC-mediated trabecular bone loss by decreasing the loss of both trabecular bone formation and osteoblast numbers. This protection appears to be conferred by LIF rescuing GC decreased activity of Stat3, MAPK, and Akt signaling pathways. Thus, the specific targeting of LIF signaling may represent a new therapeutic strategy to prevent GC-induced trabecular bone loss.}, year = {2021}, month = {apr}, issn = {1873-2763}, DOI = {10.1016/j.bone.2021.115843}, journal = {Bone}, volume = {145}, pages = {115843}, keywords = {Animals; Cell Differentiation; Glucocorticoids, toxicity; Leukemia Inhibitory Factor; Mice; Osteoblasts; Osteogenesis; Glucocorticoid-induced osteoporosis; Glucocorticoids; Leukemia inhibitory factor; Osteoblast differentiation} } @Article { 335739847135_2021, author = {Preuss, J. M. and Burret, U. and Vettorazzi, S.}, title = {Multiplex Fluorescent Bead-Based Immunoassay for the Detection of Cytokines, Chemokines, and Growth Factors}, year = {2021}, journal = {Methods Mol Biol.}, volume = {2261}, pages = {247-262} } @Article { Liao2021, author = {Liao, Nannan and Koehne, Till and Tuckermann, Jan and Triviai, Ioanna and Amling, Michael and David, Jean-Pierre and Schinke, Thorsten and Luther, Julia}, title = {Osteoblast-specific inactivation of p53 results in locally increased bone formation.}, abstract = {Inactivation of the tumor suppressor p53 (encoded by the Trp53 gene) is relevant for development and growth of different cancers, including osteosarcoma, a primary bone tumor mostly affecting children and young adolescents. We have previously shown that deficiency of the ribosomal S6 kinase 2 (Rsk2) limits osteosarcoma growth in a transgenic mouse model overexpressing the proto-oncogene c-Fos. Our initial aim for the present study was to address the question, if Rsk2 deficiency would also influence osteosarcoma growth in another mouse model. For that purpose, we took advantage of Trp53fl/fl mice, which were crossed with Runx2Cre transgenic mice in order to inactivate p53 specifically in osteoblast lineage cells. However, since we unexpectedly identified Runx2Cre-mediated recombination also in the thymus, the majority of 6-month-old Trp53fl/fl;Runx2-Cre (thereafter termed Trp53Cre) animals displayed thymic lymphomas, similar to what has been described for Trp53-deficient mice. Since we did not detect osteosarcoma formation at that age, we could not follow our initial aim, but we studied the skeletal phenotype of Trp53Cre mice, with or without additional Rsk2 deficiency. Here we unexpectedly observed that Trp53Cre mice display a unique accumulation of trabecular bone in the midshaft region of the femur and the humerus, consistent with its previously established role as a negative regulator of osteoblastogenesis. Since this local bone mass increase in Trp53Cre mice was significantly reduced by Rsk2 deficiency, we isolated bone marrow cells from the different groups of mice and analyzed their behavior ex vivo. Here we observed a remarkable increase of colony formation, osteogenic differentiation and proliferation in Trp53Cre cultures, which was unaffected by Rsk2 deficiency. Our data thereby confirm a critical and tumorigenesis-independent function of p53 as a key regulator of mesenchymal cell differentiation.}, year = {2021}, language = {eng}, journal = {PloS one}, volume = {16}, pages = {e0249894}, keywords = {Animals, Bone Neoplasms/genetics/*metabolism/pathology, Bone and Bones/metabolism/*pathology, Cancellous Bone/pathology, Carcinogenesis/genetics, Cell Proliferation, Lymphoma/genetics/*metabolism/pathology, Mice, Knockout, Osteoblasts/*metabolism, Osteogenesis/*physiology, Osteosarcoma/genetics/metabolism/pathology, Thymus Neoplasms/genetics/*metabolism/pathology, Tumor Suppressor Protein p53/genetics/*metabolism} } @Article { 672930144441_2020, author = {Wepler, M. and Preuss, J. M. and Merz, T. and McCook, O. and Radermacher, P. and Tuckermann, J. P. and Vettorazzi, S.}, title = {Impact of downstream effects of glucocorticoid receptor dysfunction on organ function in critical illness-associated systemic inflammation}, year = {2020}, month = {12}, day = {18}, journal = {Intensive Care Med Exp.}, volume = {8}, pages = {37}, number = {1} } @Article { 151379686821_2020, author = {Brazel, Christina B and Saalbach, A.}, title = {Inhibition of 11β-HSD1 Expression by Insulin in Skin: Impact for Diabetic Wound Healing}, year = {2020}, month = {11}, day = {28}, journal = {J Clin Med.}, volume = {9}, pages = {3878}, number = {12} } @Article { 458503565401_2020, author = {Stein, M. and Barnea-Zohar, M. and Shalev, M. and Arman, E. and Brenner, O. and Winograd-Katz, S. and Gerstung, J. and Thalji, F. and Kanaan, M. and Elinav, H. and Stepensky, P. and Geiger, B. and Tuckermann, J. and Elson, A.}, title = {Massive Osteopetrosis Caused by Non-Functional Osteoclasts in R51Q SNX10 Mutant Mice}, year = {2020}, month = {07}, journal = {Bone}, volume = {136}, pages = {115360} } @Article { HildebrandtBTTHR2018, author = {Hildebrandt, S. and Baschant, U. and Thiele, S. and Tuckermann, J. and Hofbauer, L.C. and Rauner, M.}, title = {Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo}, year = {2020}, month = {6}, day = {4}, journal = {Sci Rep.}, volume = {10}, pages = {9344}, number = {1} } @Article { 844142693711_2020, author = {M{\"u}ller, D. I H and Stoll, C. and Palumbo-Zerr, K. and B{\"o}hm, C. and Krishnacoumar, B. and Ipseiz, N. and Taubmann, J. and Zimmermann, M. and B{\"o}ttcher, M. and Mougiakakos, D. and Tuckermann, J. and Djouad, F. and Schett, G. and Scholtysek, C. and Kr{\"o}nke, G.}, title = {PPARδ-mediated Mitochondrial Rewiring of Osteoblasts Determines Bone Mass}, year = {2020}, month = {05}, day = {21}, journal = {Sci Rep.}, volume = {10}, pages = {8428}, number = {1} } @Article { 620508529689_2020, author = {Merz, T. and Denoix, N. and Wigger, D. and Waller, C. and Wepler, M. and Vettorazzi, S. and Tuckermann, J. and Radermacher, P. and McCook, O.}, title = {The Role of Glucocorticoid Receptor and Oxytocin Receptor in the Septic Heart in a Clinically Relevant, Resuscitated Porcine Model With Underlying Atherosclerosis}, year = {2020}, month = {05}, day = {14}, journal = {Front Endocrinol (Lausanne)}, volume = {11}, pages = {299} } @Article { 331660512019_2020, author = {Gruber, A. and M{\"u}ller, R. and Wagner, A. and Colucci, S. and Vuji{\c} Spasi{\c}, M. and Leopold, K.}, title = {Total Reflection X-ray Fluorescence Spectrometry for Trace Determination of Iron and Some Additional Elements in Biological Samples}, year = {2020}, month = {04}, day = {26}, journal = {Anal Bioanal Chem.} } @Article { 847252274482_2020, author = {Fischer-Riepe, L. and Daber, N. and Schulte-Schrepping, J. and De Carvalho, Bruna Caroline V{\'e}ras and Russo, A. and Pohlen, M. and Fischer, J. and Chasan, A. I. and Wolf, M. and Ulas, T. and Glander, S. and Schulz, C. and Skryabin, B. and Dipl. Ing. Wollbrink, A. and Steingraeber, N. and Stremmel, C. and Koehle, M. and G{\"a}rtner, F. and Vettorazzi, Sabine and Holzinger, D. and Gross, J. and Rosenbauer, F. and Stoll, M. and Niemann, S. and Tuckermann, J. and Schultze, Joachim L. and Roth, J. and Barczyk-Kahlert, K.}, title = {CD163 Expression Defines Specific, IRF8-dependent, Immune-Modulatory Macrophages in the Bone Marrow}, year = {2020}, month = {03}, day = {19}, journal = {J Allergy Clin Immunol}, volume = {S0091-6749}, pages = {30344-4}, number = {20} } @Article { 281390592558_2020, author = {Tangudu, Naveen Kumar and Yilmaz, D. and W{\"o}rle, K. and Gruber, A. and Colucci, S. and Leopold, K. and Muckenthaler, M. U. and Vuji{\c} Spasi{\c}, M.}, title = {Macrophage-HFE Controls Iron Metabolism and Immune Responses in Aged Mice}, year = {2020}, month = {02}, day = {20}, journal = {Haematologica}, volume = {haematol.2019.}, pages = {235630} } @Article { 138569274043_2020, author = {Wepler, M. and Preuss, J. M. and Merz, T. and Hartmann, C. and Wachter, U. and McCook, O. and Vogt, J. and Kress, S. and Gr{\"o}ger, M. and Fink, M. and Scheuerle, A. and M{\"o}ller, P. and Calzia, E. and Burret, U. and Radermacher, P. and Tuckermann, J. P. and Vettorazzi, S.}, title = {Impaired Glucocorticoid Receptor Dimerization Aggravates LPS-Induced Circulatory and Pulmonary Dysfunction}, year = {2020}, month = {01}, day = {23}, journal = {Front Immunol.}, volume = {10}, pages = {3152} } @Article { Brazel2020, author = {Brazel, Christina B. and Simon, Jan C. and Tuckermann, Jan P. and Saalbach, Anja}, title = {Inhibition of 11β-HSD1 Expression by Insulin in Skin: Impact for Diabetic Wound Healing.}, abstract = {Chronic, non-healing wounds impose a great burden on patients, professionals and health care systems worldwide. Diabetes mellitus (DM) and obesity are globally highly prevalent metabolic disorders and increase the risk for developing chronic wounds. Glucocorticoids (GCs) are endogenous stress hormones that exert profound effects on inflammation and repair systems. 11-beta-hydroxysteroid dehydrogenase 1 (11β-HSD1) is the key enzyme which controls local GC availability in target tissues such as skin. Since treatment with GCs has detrimental side effects on skin integrity, causing atrophy and delayed wound healing, we asked whether the dysregulated expression of 11β-HSD1 and consequently local GC levels in skin contribute to delayed wound healing in obese, diabetic db/db mice. We found increased expression of 11β-HSD1 during disturbed wound healing and in the healthy skin of obese, diabetic db/db mice. Cell analysis revealed increased expression of 11β-HSD1 in fibroblasts, myeloid cells and dermal white adipose tissue from db/db mice, while expression in keratinocytes was unaffected. Among diabetes- and obesity-related factors, insulin and insulin-like growth factor 1 down-regulated 11β-HSD1 expression in fibroblasts and myeloid cells, while glucose, fatty acids, TNF-α and IL-1β did not affect it. Insulin exerted its inhibitory effect on 11β-HSD1 expression by activating PI3-kinase/Akt-signalling. Consequently, the inhibitory effect of insulin is attenuated in fibroblasts from insulin-resistant db/db mice. We conclude that insulin resistance in obesity and diabetes prevents the down-regulation of 11β-HSD1, leading to elevated endogenous GC levels in diabetic skin, which could contribute to impaired wound healing in patients with DM.}, year = {2020}, month = {nov}, issn = {2077-0383}, DOI = {10.3390/jcm9123878}, journal = {Journal of clinical medicine}, volume = {9}, keywords = {11-beta-hydroxysteroid dehydrogenase; corticosterone; diabetes mellitus; fibroblasts; insulin; obesity; skin; wound healing} } @Article { FischerRiepe2020, author = {Fischer-Riepe, Lena and Daber, Niklas and Schulte-Schrepping, Jonas and V{\'e}ras De Carvalho, Bruna Caroline and Russo, Antonella and Pohlen, Michele and Fischer, Josephine and Chasan, Achmet Imam and Wolf, Marc and Ulas, Thomas and Glander, Shirin and Schulz, Christian and Skryabin, Boris and Wollbrink Dipl-Ing, Andreas and Steingraeber, Nadine and Stremmel, Christopher and Koehle, Megan and G{\"a}rtner, Florian and Vettorazzi, Sabine and Holzinger, Dirk and Gross, Joachim and Rosenbauer, Frank and Stoll, Monika and Niemann, Silke and Tuckermann, Jan and Schultze, Joachim L. and Roth, Johannes and Barczyk-Kahlert, Katarzyna}, title = {CD163 expression defines specific, IRF8-dependent, immune-modulatory macrophages in the bone marrow.}, abstract = {Scavenger receptor CD163 is exclusively expressed on monocytes/macrophages and is widely used as a marker for alternatively activated macrophages. However, the role of CD163 is not yet clear. We sought to examine the function of CD163 in steady-state as well as in sterile and infectious inflammation. Expression of CD163 was analyzed under normal and inflammatory conditions in mice. Functional relevance of CD163 was investigated in models of inflammation in wild-type and CD163 mice. We describe a subpopulation of bone marrow-resident macrophages (BMRMs) characterized by a high expression of CD163 and functionally distinct from classical bone marrow-derived macrophages. Development of CD163 BMRMs is strictly dependent on IFN regulatory factor-8. CD163 BMRMs show a specific transcriptome and cytokine secretion pattern demonstrating a specific immunomodulatory profile of these cells. Accordingly, CD163 mice show a stronger inflammation in allergic contact dermatitis, indicating a regulatory role of CD163. However, CD163 mice are highly susceptible to S aureus infections, demonstrating the relevance of CD163 for antimicrobial defense as well. Our data indicate that anti-inflammatory and immunosuppressive mechanisms are not necessarily associated with a decreased antimicrobial activity. In contrast, our data define a novel macrophage population that controls overwhelming inflammation on one hand but is also necessary for an effective control of infections on the other hand.}, year = {2020}, month = {nov}, issn = {1097-6825}, DOI = {10.1016/j.jaci.2020.02.034}, journal = {The Journal of allergy and clinical immunology}, volume = {146}, pages = {1137--1151}, keywords = {Animals; Antigens, CD, genetics, metabolism; Antigens, Differentiation, Myelomonocytic, genetics, metabolism; Bone Marrow Cells, immunology, metabolism; Cells, Cultured; Cytokines, metabolism; Dermatitis, Allergic Contact, immunology; Disease Models, Animal; Disease Susceptibility; Humans; Immunomodulation; Inflammation, immunology; Interferon Regulatory Factors, genetics, metabolism; Macrophage Activation; Macrophages, immunology, metabolism; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Receptors, Cell Surface, genetics, metabolism; Staphylococcal Infections, immunology; Staphylococcus aureus, physiology; Transcriptome; IFN regulatory factor 8; Resident bone marrow macrophages; scavenger receptor CD163; sterile and systemic inflammation} } @Article { Hachemi2020, author = {Hachemi, Yasmine and Rapp, Anna E. and Lee, Sooyeon and Dorn, Ann-Kristin and Kr{\"u}ger, Benjamin T. and Kaiser, Kathrin and Ignatius, Anita and Tuckermann, Jan}, title = {Intact Glucocorticoid Receptor Dimerization Is Deleterious in Trauma-Induced Impaired Fracture Healing.}, abstract = {Following severe trauma, fracture healing is impaired because of overwhelming systemic and local inflammation. Glucocorticoids (GCs), acting the glucocorticoid receptor (GR), influence fracture healing by modulating the trauma-induced immune response. GR dimerization-dependent gene regulation is essential for the anti-inflammatory effects of GCs. Therefore, we investigated in a murine trauma model of combined femur fracture and thoracic trauma, whether effective GR dimerization influences the pathomechanisms of trauma-induced compromised fracture healing. To this end, we used mice with decreased GR dimerization ability (GR ). The healing process was analyzed by cytokine/chemokine multiplex analysis, flow cytometry, gene-expression analysis, histomorphometry, micro-computed tomography, and biomechanical testing. GR mice did not display a systemic or local hyper-inflammation upon combined fracture and thorax trauma. Strikingly, we discovered that GR mice were protected from fracture healing impairment induced by the additional thorax trauma. Collectively and in contrast to previous studies describing the beneficial effects of intact GR dimerization in inflammatory models, we report here an adverse role of intact GR dimerization in trauma-induced compromised fracture healing.}, year = {2020}, issn = {1664-3224}, DOI = {10.3389/fimmu.2020.628287}, journal = {Frontiers in immunology}, volume = {11}, pages = {628287}, keywords = {Animals; Fracture Healing, genetics, immunology; Male; Mice; Mice, Transgenic; Protein Multimerization, genetics, immunology; Receptors, Glucocorticoid, genetics, immunology; Thoracic Injuries, genetics, immunology, pathology; bone repair; fracture; glucocorticoid receptor; inflammation; thoracic trauma} } @Article { Merz2020, author = {Merz, Tamara and Denoix, Nicole and Wigger, Daniela and Waller, Christiane and Wepler, Martin and Vettorazzi, Sabine and Tuckermann, Jan and Radermacher, Peter and McCook, Oscar}, title = {The Role of Glucocorticoid Receptor and Oxytocin Receptor in the Septic Heart in a Clinically Relevant, Resuscitated Porcine Model With Underlying Atherosclerosis.}, abstract = {The pathophysiology of sepsis-induced myocardial dysfunction is not resolved to date and comprises inflammation, barrier dysfunction and oxidative stress. Disease-associated reduction of tissue cystathionine-γ-lyase (CSE) expression, an endogenous H S-producing enzyme, is associated with oxidative stress, barrier dysfunction and organ injury. CSE-mediated cardio-protection has been suggested to be related the upregulation of oxytocin receptor (OTR). CSE can also mediate glucocorticoid receptor (GR) signaling, which is important for normal heart function. A sepsis-related loss of cardiac CSE expression associated with impaired organ function has been reported previously. The aim of this current study was to investigate the role of cardiac GR and OTR after polymicrobial sepsis in a clinically relevant, resuscitated, atherosclerotic porcine model. Anesthetized and instrumented FBM (Familial Hypercholesterolemia Bretoncelles Meishan) pigs with high fat diet-induced atherosclerosis underwent poly-microbial septic shock ( = 8) or sham procedure ( = 5), and subsequently received intensive care therapy with fluid and noradrenaline administration for 24 h. Cardiac protein expression and mRNA levels were analyzed. Systemic troponin, a marker of cardiac injury, was significantly increased in septic animals in contrast to sham, whereas OTR and GR expression in septic hearts were reduced, along with a down-regulation of anti-inflammatory GR target genes and the antioxidant transcription factor NRF2. These results suggest a potential interplay between GR, CSE, and OTR in sepsis-mediated oxidative stress, inflammation and cardiac dysfunction.}, year = {2020}, issn = {1664-2392}, DOI = {10.3389/fendo.2020.00299}, journal = {Frontiers in endocrinology}, volume = {11}, pages = {299}, keywords = {Animals; Atherosclerosis, physiopathology; Cystathionine gamma-Lyase, genetics, metabolism; Disease Models, Animal; Gene Expression Regulation; Heart Diseases, etiology, metabolism, pathology; Hydrogen Sulfide, metabolism; Hypercholesterolemia, physiopathology; Male; Oxidative Stress; Receptors, Glucocorticoid, genetics, metabolism; Receptors, Oxytocin, genetics, metabolism; Shock, Septic, complications; Signal Transduction; Swine; cystathionine-γ-lyase; glucocorticoid receptor; heart; inflammation; oxidative stress; oxytocin receptor; sepsis} } @Article { Hildebrandt2020, author = {Hildebrandt, Susanne and Baschant, Ulrike and Thiele, Sylvia and Tuckermann, Jan and Hofbauer, Lorenz C. and Rauner, Martina}, title = {Author Correction: Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo.}, abstract = {An amendment to this paper has been published and can be accessed via a link at the top of the paper.}, year = {2020}, month = {jun}, issn = {2045-2322}, DOI = {10.1038/s41598-020-65962-6}, journal = {Scientific reports}, volume = {10}, pages = {9344} } @Article { Mueller2020, author = {M{\"u}ller, Dorothea I. H. and Stoll, Cornelia and Palumbo-Zerr, Katrin and B{\"o}hm, Christina and Krishnacoumar, Brenda and Ipseiz, Natacha and Taubmann, Jule and Zimmermann, Max and B{\"o}ttcher, Martin and Mougiakakos, Dimitrios and Tuckermann, Jan and Djouad, Farida and Schett, Georg and Scholtysek, Carina and Kr{\"o}nke, Gerhard}, title = {PPARδ-mediated mitochondrial rewiring of osteoblasts determines bone mass.}, abstract = {Bone turnover, which is determined by osteoclast-mediated bone resorption and osteoblast-mediated bone formation, represents a highly energy consuming process. The metabolic requirements of osteoblast differentiation and mineralization, both essential for regular bone formation, however, remain incompletely understood. Here we identify the nuclear receptor peroxisome proliferator-activated receptor (PPAR) δ as key regulator of osteoblast metabolism. Induction of PPARδ was essential for the metabolic adaption and increased rate in mitochondrial respiration necessary for the differentiation and mineralization of osteoblasts. Osteoblast-specific deletion of PPARδ in mice, in turn, resulted in an altered energy homeostasis of osteoblasts, impaired mineralization and reduced bone mass. These data show that PPARδ acts as key regulator of osteoblast metabolism and highlight the relevance of cellular metabolic rewiring during osteoblast-mediated bone formation and bone-turnover.}, year = {2020}, month = {may}, issn = {2045-2322}, DOI = {10.1038/s41598-020-65305-5}, journal = {Scientific reports}, volume = {10}, pages = {8428}, keywords = {Animals; Bone Density, physiology; Bone Remodeling, physiology; Cell Differentiation; Cells, Cultured; Energy Metabolism, genetics, physiology; Mesenchymal Stem Cells, cytology; Mice; Mice, Knockout; Mitochondria, metabolism; Osteoblasts, cytology, metabolism; Osteoclasts, metabolism; Osteogenesis, physiology; Oxidative Phosphorylation; PPAR delta, genetics, metabolism} } @Article { 972006866175_2020, author = {Datzmann, T. and Hoffmann, A. and McCook, O. and Merz, T. and Wachter, U. and Preuss, J. and Vettorazzi, S. and Calzia, E. and Gr{\"o}ger, M. and Kohn, F. and Schmid, A. and Denoix, N. and Radermacher, P. and Wepler, M.}, title = {Effects of sodium thiosulfate (Na2S2O3) during resuscitation from hemorrhagic shock in swine with preexisting atherosclerosis}, year = {2020}, month = {01}, journal = {Pharmacol Res.}, volume = {151}, pages = {104536} } @Article { Stein2020, author = {Stein, Merle and Barnea-Zohar, Maayan and Shalev, Moran and Arman, Esther and Brenner, Ori and Winograd-Katz, Sabina and Gerstung, Jennifer and Thalji, Fadi and Kanaan, Moien and Elinav, Hila and Stepensky, Polina and Geiger, Benjamin and Tuckermann, Jan and Elson, Ari}, title = {Massive osteopetrosis caused by non-functional osteoclasts in R51Q SNX10 mutant mice.}, abstract = {The R51Q mutation in sorting nexin 10 (SNX10) was shown to cause a lethal genetic disease in humans, namely autosomal recessive osteopetrosis (ARO). We describe here the first R51Q SNX10 knock-in mouse model and show that mice homozygous for this mutation exhibit massive, early-onset, and widespread osteopetrosis. The mutant mice exhibit multiple additional characteristics of the corresponding human disease, including stunted growth, failure to thrive, missing or impacted teeth, occasional osteomyelitis, and a significantly-reduced lifespan. Osteopetrosis in this model is the result of osteoclast inactivity that, in turn, is caused by absence of ruffled borders in the mutant osteoclasts and by their inability to secrete protons. These results confirm that the R51Q mutation in SNX10 is a causative factor in ARO and provide a model system for studying this rare disease.}, year = {2020}, month = {jul}, issn = {1873-2763}, DOI = {10.1016/j.bone.2020.115360}, journal = {Bone}, volume = {136}, pages = {115360}, keywords = {Animals; Mice; Mutation, genetics; Osteoclasts; Osteopetrosis, diagnostic imaging, genetics; Sorting Nexins, genetics; Autosomal recessive osteopetrosis; Osteoclast; Osteopetrosis; SNX10; Sorting nexin 10} } @Article { Wepler2020, author = {Wepler, Martin and Preuss, Jonathan M. and Merz, Tamara and McCook, Oscar and Radermacher, Peter and Tuckermann, Jan P. and Vettorazzi, Sabine}, title = {Impact of downstream effects of glucocorticoid receptor dysfunction on organ function in critical illness-associated systemic inflammation.}, abstract = {Glucocorticoids (GCs) are stress hormones that regulate developmental and physiological processes and are among the most potent anti-inflammatory drugs to suppress chronic and acute inflammation. GCs act through the glucocorticoid receptor (GR), a ubiquitously expressed ligand-activated transcription factor, which translocates into the nucleus and can act via two different modes, as a GR monomer or as a GR dimer. These two modes of action are not clearly differentiated in practice and may lead to completely different therapeutic outcomes. Detailed aspects of GR mechanisms are often not taken into account when GCs are used in different clinical scenarios. Patients, with critical illness-related corticosteroid insufficiency, treated with natural or synthetic GCs are still missing a clearly defined therapeutic strategy. This review discusses the different modes of GR function and its importance on organ function in vivo.}, year = {2020}, month = {dec}, issn = {2197-425X}, DOI = {10.1186/s40635-020-00325-z}, journal = {Intensive care medicine experimental}, volume = {8}, pages = {37}, keywords = {Dimer; Dysfunction; Glucocorticoid receptor; Monomer; Mouse models; Organ function; Systemic inflammation} } @Article { 221103966325_2019, author = {Conaway, H. H. and Henning, P. and Lie, A. and Tuckermann, J. and Lerner, U. H.}, title = {Glucocorticoids employ the monomeric glucocorticoid receptor to potentiate vitamin D3 and parathyroid hormone-induced osteoclastogenesis}, year = {2019}, month = {12}, journal = {FASEB J.}, volume = {33}, pages = {14394-14409}, number = {12} } @Article { 268930434529_2019, author = {Ahmad, M. and Hachemi, Y. and Paxian, K. and Mengele, F. and Koenen, M. and Tuckermann, J.}, title = {A Jack of All Trades: Impact of Glucocorticoids on Cellular Cross-Talk in Osteoimmunology}, year = {2019}, month = {10}, day = {17}, journal = {Front Immunol.}, volume = {10}, pages = {2460} } @Article { 930741455471_2019, author = {Herdoiza Padilla, E. and Crauwels, P. and Bergner, T. and Wiederspohn, N. and F{\"o}rstner, S. and Rinas, R. and Ruf, A. and Kleemann, M. and Handrick, R. and Tuckermann, J. and Otte, K. and Walther, P. and Riedel, CU.}, title = {mir-124-5p Regulates Phagocytosis of Human Macrophages by Targeting the Actin Cytoskeleton via the ARP2/3 Complex}, year = {2019}, month = {10}, day = {04}, journal = {Front Immunol.}, pages = {2210}, number = {10} } @Article { 961242077198_2019, author = {Kroll, T. and Ahmad, M. and Ploubidou, A. and Tuckermann, J.}, title = {RNAi-Screening in Knochenbildenden Zellen}, year = {2019}, month = {09}, day = {03}, journal = {BIOspektrum} } @Article { 247854863760_2019, author = {Escoter-Torres, L. and Caratti, G. and Mechtidou, A. and Tuckermann, J. and Uhlenhaut, N. H. and Vettorazzi, S.}, title = {Fighting the Fire: Mechanisms of Inflammatory Gene Regulation by the Glucocorticoid Receptor}, year = {2019}, month = {08}, day = {07}, journal = {Front Immunol.}, pages = {1859}, number = {10} } @Article { 411055324946_2019, author = {Wagner, A. and Alan, B. and Yilmaz, D. and Ahmad, M. and Liu, P. and Tangudu, NK. and Tuckermann, J. P. and Vuji{\c} Spasi{\c}, M.}, title = {Despite Genetic Iron Overload, Hfe-Hemochromatosis Mice Do Not Show Bone Loss}, year = {2019}, month = {07}, day = {26}, journal = {JBMR Plus}, volume = {3}, pages = {e10206}, number = {9} } @Article { 640616589064_2019, author = {Mov{\'e}rare-Skrtic, S. and Nilsson, KH. and Henning, P. and Funck-Brentano, T. and Nethander, M. and Rivadeneira, F. and Coletto Nunes, G. and Koskela, A. and Tuukkanen, J. and Tuckermann, J. and Perret, C. and Souza, PPC. and Lerner, U. H. and Ohlsson, C.}, title = {Osteoblast-derived NOTUM reduces cortical bone mass in mice and the NOTUM locus is associated with bone mineral density in humans}, year = {2019}, month = {07}, day = {15}, journal = {FASEB J.}, volume = {33}, pages = {11163-11179}, number = {10} } @Article { PfanderFBLV2019, author = {Pf{\"a}nder, P. and Fidan, Miray and Burret, U. and Lipinski, Lena and Vettorazzi, Sabine}, title = {Cdk5 Deletion Enhances the Anti-inflammatory Potential of GC-Mediated GR Activation During Inflammation}, year = {2019}, month = {7}, day = {10}, journal = {Front. Immunol.}, volume = {10}, pages = {1554}, number = {10} } @Article { 676253141190_2019, author = {Desgeorges, T. and Caratti, G. and Mounier, R. and Tuckermann, J. and Chazaud, B.}, title = {Glucocorticoids Shape Macrophage Phenotype for Tissue Repair}, year = {2019}, month = {07}, day = {09}, journal = {Front Immunol.}, pages = {1591}, number = {10} } @Article { vanWeertBSVMHPZSRTSM2019, author = {van Weert, LTCM. and Buurstede, JC. and Sips, HCM. and Vettorazzi, S. and Mol, IM. and Hartmann, J. and Prekovic, S. and Zwart, W. and Schmidt, MV. and Roozendaal, B. and Tuckermann, JP. and Sarabdjitsingh, RA. and Meijer, OC.}, title = {Identification of mineralocorticoid receptor target genes in the mouse hippocampus}, year = {2019}, month = {5}, day = {23}, journal = {J Neuroendocrinol.}, pages = {e12735}, number = {8} } @Article { TanguduBSCS2019, author = {Tangudu, NK. and Buth, N. and Strnad, P. and Cirstea, IC. and Spasic´, MV.}, title = {Deregulation of Hepatic Mek1/2⁻Erk1/2 Signaling Module in Iron Overload Conditions}, year = {2019}, month = {5}, day = {7}, journal = {Pharmaceuticals (Basel)}, volume = {7}, pages = {2}, number = {12} } @Article { GlantschnigKGKPWPCGHVBTUHS2019, author = {Glantschnig, C. and Koenen, M. and Gil-Lozano, M. and Karbiener, M. and Pickrahn, I. and Williams-Dautovich, J. and Patel, R. and Cummins, CL. and Giroud, M. and Hartleben, G. and Vogl, E. and Bl{\"u}her, M. and Tuckermann, J. and Uhlenhaut, H. and Herzig, S. and Scheideler, M.}, title = {A miR-29a-driven negative feedback loop regulates peripheral glucocorticoid receptor signaling}, year = {2019}, month = {2}, day = {11}, journal = {FASEB J.}, volume = {33}, pages = {5924-5941}, number = {5} } @Article { RothWWSASBSBTE2019, author = {Roth, L. and Wakim, J. and Wasserman, E. and Shalev, M. and Arman, E. and Stein, M. and Brumfeld, V. and Sagum, CA. and Bedford, MT. and Tuckermann, J. and Elson, A.}, title = {Phosphorylation of the phosphatase PTPROt at Tyr399 is a molecular switch that controls osteoclast activity and bone mass in vivo}, year = {2019}, month = {1}, day = {8}, journal = {Sci Signal}, volume = {8}, pages = {563}, number = {12} } @Article { MoverareSkrtic2019, author = {Mov{\'e}rare-Skrtic, Sofia and Nilsson, Karin H. and Henning, Petra and Funck-Brentano, Thomas and Nethander, Maria and Rivadeneira, Fernando and Coletto Nunes, Glaucia and Koskela, Antti and Tuukkanen, Juha and Tuckermann, Jan and Perret, Christine and Souza, Pedro Paulo Chaves and Lerner, Ulf H. and Ohlsson, Claes}, title = {Osteoblast-derived NOTUM reduces cortical bone mass in mice and the , javax.xml.bind.JAXBElement@5166fe8c, locus is associated with bone mineral density in humans.}, abstract = {Osteoporosis is a common skeletal disease, affecting millions of individuals worldwide. Currently used osteoporosis treatments substantially reduce vertebral fracture risk, whereas nonvertebral fracture risk, mainly caused by reduced cortical bone mass, has only moderately been improved by the osteoporosis drugs used, defining an unmet medical need. Because several wingless-type MMTV integration site family members (WNTs) and modulators of WNT activity are major regulators of bone mass, we hypothesized that NOTUM, a secreted WNT lipase, might modulate bone mass an inhibition of WNT activity. To characterize the possible role of endogenous NOTUM as a physiologic modulator of bone mass, we developed global, cell-specific, and inducible -inactivated mouse models. expression was high in the cortical bone in mice, and conditional inactivation revealed that osteoblast lineage cells are the principal source of NOTUM in the cortical bone. Osteoblast lineage-specific inactivation increased cortical bone thickness an increased periosteal circumference. Inducible inactivation in adult mice increased cortical bone thickness as a result of increased periosteal bone formation, and silencing of expression in cultured osteoblasts enhanced osteoblast differentiation. Large-scale human genetic analyses identified genetic variants mapping to the locus that are strongly associated with bone mineral density (BMD) as estimated with quantitative ultrasound in the heel. Thus, osteoblast-derived NOTUM is an essential local physiologic regulator of cortical bone mass effects on periosteal bone formation in adult mice, and genetic variants in the locus are associated with BMD variation in adult humans. Therapies targeting osteoblast-derived NOTUM may prevent nonvertebral fractures.-Mov{\'e}rare-Skrtic, S., Nilsson, K. H., Henning, P., Funck-Brentano, T., Nethander, M., Rivadeneira, F., Coletto Nunes, G., Koskela, A., Tuukkanen, J., Tuckermann, J., Perret, C., Souza, P. P. C., Lerner, U. H., Ohlsson, C. Osteoblast-derived NOTUM reduces cortical bone mass in mice and the locus is associated with bone mineral density in humans.}, year = {2019}, month = {oct}, issn = {1530-6860}, DOI = {10.1096/fj.201900707R}, journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology}, volume = {33}, pages = {11163--11179}, keywords = {Animals; Bone Density, genetics, physiology; Cell Differentiation, genetics, physiology; Cortical Bone, metabolism, physiology; Esterases, genetics, metabolism; Female; Fractures, Bone, metabolism, physiopathology; Genetic Variation, genetics; Humans; Male; Mice; Osteoblasts, metabolism; Osteogenesis, genetics, physiology; Osteoporosis, metabolism, physiopathology; Wnt Proteins, metabolism; WNT16; osteoporosis; transgenic} } @Article { HerdoizaPadilla2019, author = {Herdoiza Padilla, Estefania and Crauwels, Peter and Bergner, Tim and Wiederspohn, Nicole and F{\"o}rstner, Sabrina and Rinas, Rebecca and Ruf, Anna and Kleemann, Michael and Handrick, Ren{\'e} and Tuckermann, Jan and Otte, Kerstin and Walther, Paul and Riedel, Christian U.}, title = {mir-124-5p Regulates Phagocytosis of Human Macrophages by Targeting the Actin Cytoskeleton via the ARP2/3 Complex.}, abstract = {Phagocytosis is a cellular process crucial for recognition and removal of apoptotic cells and foreign particles, subsequently initiating appropriate immune responses. The process of phagocytosis is highly complex and involves major rearrangements of the cytoskeleton. Due to its complexity and importance for tissue homoeostasis and immune responses, it is tightly regulated. Over the last decade, microRNAs (miRNAs) have emerged as important regulators of biological pathways including the immune response by fine-tuning expression of gene regulatory networks. In order to identify miRNAs implicated in the regulation of phagocytosis, a systematic screening of all currently known, human miRNAs was performed using THP-1 macrophage-like cells and serum-opsonized latex beads. Of the total of 2,566 miRNAs analyzed, several led to significant changes in phagocytosis. Among these, we validated miR-124-5p as a novel regulator of phagocytosis. Transfection with miR-124-5p mimics reduced the number of phagocytic cells as well as the phagocytic activity of phorbol-12-myristate-13-acetate (PMA)-activated THP-1 cells and differentiated primary human macrophages. analysis suggested that miR-124-5p targets genes involved in regulation of the actin cytoskeleton. Transcriptional analyses revealed that expression of genes encoding for several subunits of the ARP2/3 complex, a crucial regulator of actin polymerization, is reduced upon transfection of cells with miR-124-5p. Further analyses identified potential binding motifs for miR-124-5p in the mRNAs of these genes. Luciferase reporter assays using these binding motifs indicate that at least two of the genes ( and ) are direct targets of miR-124-5p. Moreover, ARPC3 and ARPC4 protein levels were significantly reduced following miR-124-5p transfection. Collectively, the presented results suggest that miR-124-5p regulates phagocytosis in human macrophages by directly targeting expression of components of the ARP2/3 complex.}, year = {2019}, issn = {1664-3224}, DOI = {10.3389/fimmu.2019.02210}, journal = {Frontiers in immunology}, volume = {10}, pages = {2210}, keywords = {Actin Cytoskeleton, physiology; Actin-Related Protein 2-3 Complex, physiology; HEK293 Cells; Humans; Macrophages, immunology; MicroRNAs, physiology; Phagocytosis; THP-1 Cells; ARP2/3; high-content screening; macrophage; microRNA; phagocytosis} } @Article { Javaheri2019, author = {Javaheri, Tahereh and Kazemi, Zahra and Pencik, Jan and Pham, Ha T. T. and Kauer, Maximilian and Noorizadeh, Rahil and Sax, Barbara and Nivarthi, Harini and Schlederer, Michaela and Maurer, Barbara and Hofbauer, Maximillian and Aryee, Dave N. T. and Wiedner, Marc and Tomazou, Eleni M. and Logan, Malcolm and Hartmann, Christine and Tuckermann, Jan P. and Kenner, Lukas and Mikula, Mario and Dolznig, Helmut and {\"U}ren, Aykut and Richter, G{\"u}nther H. and Grebien, Florian and Kovar, Heinrich and Moriggl, Richard}, title = {Retraction Note: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation.}, abstract = {An amendment to this paper has been published and can be accessed via a link at the top of the paper.}, year = {2019}, month = {aug}, issn = {2041-4889}, DOI = {10.1038/s41419-019-1853-1}, journal = {Cell death {\\&} disease}, volume = {10}, pages = {605} } @Article { Tangudu2019, author = {Tangudu, Naveen Kumar and Buth, Nils and Strnad, Pavel and Cirstea, Ion C. and Spasic, Maja Vujic}, title = {Deregulation of Hepatic Mek1/2⁻Erk1/2 Signaling Module in Iron Overload Conditions.}, abstract = {The liver, through the production of iron hormone hepcidin, controls body iron levels. High liver iron levels and deregulated hepcidin expression are commonly observed in many liver diseases including highly prevalent genetic iron overload disorders. In spite of a number of breakthrough investigations into the signals that control hepcidin expression, little progress has been made towards investigations into intracellular signaling in the liver under excess of iron. This study examined hepatic signaling pathways underlying acquired and genetic iron overload conditions. Our data demonstrate that hepatic iron overload associates with a decline in the activation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (Erk) kinase (Mek1/2) pathway by selectively affecting the phosphorylation of Erk1/2. We propose that Mek1/2-Erk1/2 signaling is uncoupled from iron-Bmp-Smad-mediated hepcidin induction and that it may contribute to a number of liver pathologies in addition to toxic effects of iron. We believe that our findings will advance the understanding of cellular signaling events in the liver during iron overload of different etiologies.}, year = {2019}, month = {may}, issn = {1424-8247}, DOI = {10.3390/ph12020070}, journal = {Pharmaceuticals (Basel, Switzerland)}, volume = {12}, keywords = {Bmp/Smad; Hfe; Mek/Erk; hepcidin; iron; liver} } @Article { Wepler2019, author = {Wepler, Martin and Preuss, Jonathan M. and Merz, Tamara and Hartmann, Clair and Wachter, Ulrich and McCook, Oscar and Vogt, Josef and Kress, Sandra and Gr{\"o}ger, Michael and Fink, Marina and Scheuerle, Angelika and M{\"o}ller, Peter and Calzia, Enrico and Burret, Ute and Radermacher, Peter and Tuckermann, Jan P. and Vettorazzi, Sabine}, title = {Impaired Glucocorticoid Receptor Dimerization Aggravates LPS-Induced Circulatory and Pulmonary Dysfunction.}, abstract = {Sepsis, that can be modeled by LPS injections, as an acute systemic inflammation syndrome is the most common cause for acute lung injury (ALI). ALI induces acute respiratory failure leading to hypoxemia, which is often associated with multiple organ failure (MOF). During systemic inflammation, the hypothalamus-pituitary-adrenal axis (HPA) is activated and anti-inflammatory acting glucocorticoids (GCs) are released to overcome the inflammation. GCs activate the GC receptor (GR), which mediates its effects via a GR monomer or GR dimer. The detailed molecular mechanism of the GR in different inflammatory models and target genes that might be crucial for resolving inflammation is not completely identified. We previously observed that mice with attenuated GR dimerization (GR ) had a higher mortality in a non-resuscitated lipopolysaccharide (LPS)- and cecal ligation and puncture (CLP)-induced inflammation model and are refractory to exogenous GCs to ameliorate ALI during inflammation. Therefore, we hypothesized that impaired murine GR dimerization (GR ) would further impair organ function in LPS-induced systemic inflammation under human like intensive care management and investigated genes that are crucial for lung function in this setup. Anesthetized GR and wildtype (GR ) mice were challenged with LPS (10 mg·kg , intraperitoneal) and underwent intensive care management ({\dq}lung-protective{\dq} mechanical ventilation, crystalloids, and norepinephrine) for 6 h. Lung mechanics and gas exchange were assessed together with systemic hemodynamics, acid-base status, and mitochondrial oxygen consumption (JO ). Western blots, immunohistochemistry, and real time quantitative polymerase chain reaction were performed to analyze lung tissue and inflammatory mediators were analyzed in plasma and lung tissue. When animals were challenged with LPS and subsequently resuscitated under intensive care treatment, GR mice had a higher mortality compared to GR mice, induced by an increased need of norepinephrine to achieve hemodynamic targets. After challenge with LPS, GR mice also displayed an aggravated ALI shown by a more pronounced impairment of gas exchange, lung mechanics and increased osteopontin (Opn) expression in lung tissue. Impairment of GR dimerization aggravates systemic hypotension and impairs lung function during LPS-induced endotoxic shock in mice. We demonstrate that the GR dimer is an important mediator of hemodynamic stability and lung function, possibly through regulation of Opn, during LPS-induced systemic inflammation.}, year = {2019}, issn = {1664-3224}, DOI = {10.3389/fimmu.2019.03152}, journal = {Frontiers in immunology}, volume = {10}, pages = {3152}, keywords = {Acute Lung Injury, etiology, metabolism; Animals; Dimerization; Lipopolysaccharides, toxicity; Mice; Protein Multimerization; Receptors, Glucocorticoid, chemistry, metabolism; Shock, Septic, complications, metabolism, physiopathology; endotoxic shock; glucocorticoid receptor; inflammation; lung function; osteopontin} } @Article { Wagner2019, author = {Wagner, Alessa and Alan, Bet{\"u}l and Yilmaz, Dilay and Ahmad, Mubashir and Liu, Peng and Tangudu, Naveen Kumar and Tuckermann, Jan P. and Vujic Spasic, Maja}, title = {Despite Genetic Iron Overload, , javax.xml.bind.JAXBElement@e709a68, -Hemochromatosis Mice Do Not Show Bone Loss.}, abstract = {One of the most prevalent genetic iron overload disorders in Caucasians is caused by mutations in the gene. Both patients and -mouse models develop a progressive accumulation of iron in the parenchymal cells of various tissues, eventually resulting in liver cirrhosis, hepatocellular carcinoma, cardiomyopathies, hypogonadism, and other pathologies. Clinical data and preclinical models have brought considerable attention to the correlation between iron overload and the development of osteoporosis in hemochromatosis. Our study critically challenges this concept. We show that systemic iron overload, at the degree present in mice, does not associate with the microarchitecture impairment of long bones, thus excluding a negative effect of iron overload on bone integrity. We further reveal that Hfe actions in osteoblasts and osteoclasts are dispensable for the maintenance of bone and iron homeostasis in mice under steady-state conditions. We conclude that, despite systemic iron overload, mice present normal physiological bone homeostasis. © 2019 The Authors. in published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.}, year = {2019}, month = {sep}, issn = {2473-4039}, DOI = {10.1002/jbm4.10206}, journal = {JBMR plus}, volume = {3}, pages = {e10206}, keywords = {BONE; HFE‐HEMOCHROMATOSIS; IRON; OSTEOBLAST/OSTEOCLASTS; OSTEOPOROSIS} } @Article { Weert2019, author = {Weert, Lisa T. C. M. and Buurstede, Jacobus C. and Sips, Hetty C. M. and Vettorazzi, Sabine and Mol, Isabel M. and Hartmann, Jakob and Prekovic, Stefan and Zwart, Wilbert and Schmidt, Mathias V. and Roozendaal, Benno and Tuckermann, Jan P. and Sarabdjitsingh, R. Angela and Meijer, Onno C.}, title = {Identification of mineralocorticoid receptor target genes in the mouse hippocampus.}, abstract = {Brain mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) respond to the same glucocorticoid hormones but can have differential effects on cellular function. Several lines of evidence suggest that MR-specific target genes must exist and might underlie the distinct effects of the receptors. The present study aimed to identify MR-specific target genes in the hippocampus, a brain region where MR and GR are co-localised and play a role in the stress response. Using genome-wide binding of both receptor types, we previously identified MR-specific, MR-GR overlapping and GR-specific putative target genes. We now report altered gene expression levels of such genes in the hippocampus of forebrain MR knockout (fbMRKO) mice, killed at the time of their endogenous corticosterone peak. Of those genes associated with MR-specific binding, the most robust effect was a 50% reduction in Jun dimerization protein 2 (Jdp2) mRNA levels in fbMRKO mice. Down-regulation was also observed for the MR-specific Nitric oxide synthase 1 adaptor protein (Nos1ap) and Suv3 like RNA helicase (Supv3 l1). Interestingly, the classical glucocorticoid target gene FK506 binding protein 5 (Fkbp5), which is associated with MR and GR chromatin binding, was expressed at substantially lower levels in fbMRKO mice. Subsequently, hippocampal Jdp2 was confirmed to be up-regulated in a restraint stress model, posing Jdp2 as a bona fide MR target that is also responsive in an acute stress condition. Thus, we show that MR-selective DNA binding can reveal functional regulation of genes and further identify distinct MR-specific effector pathways.}, year = {2019}, month = {aug}, issn = {1365-2826}, DOI = {10.1111/jne.12735}, journal = {Journal of neuroendocrinology}, volume = {31}, pages = {e12735}, keywords = {Animals; Binding Sites, genetics; Female; Gene Expression Regulation; Hippocampus, metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, Glucocorticoid, genetics, metabolism; Receptors, Mineralocorticoid, genetics, physiology; Jdp2 ; glucocorticoids; mineralocorticoid receptor knockout; restraint stress; transcription} } @Article { Ahmad2019, author = {Ahmad, Mubashir and Hachemi, Yasmine and Paxian, Kevin and Mengele, Florian and Koenen, Mascha and Tuckermann, Jan}, title = {A Jack of All Trades: Impact of Glucocorticoids on Cellular Cross-Talk in Osteoimmunology.}, abstract = {Glucocorticoids (GCs) are known to have a strong impact on the immune system, metabolism, and bone homeostasis. While these functions have been long investigated separately in immunology, metabolism, or bone biology, the understanding of how GCs regulate the cellular cross-talk between innate immune cells, mesenchymal cells, and other stromal cells has been garnering attention rather recently. Here we review the recent findings of GC action in osteoporosis, inflammatory bone diseases (rheumatoid and osteoarthritis), and bone regeneration during fracture healing. We focus on studies of pre-clinical animal models that enable dissecting the role of GC actions in innate immune cells, stromal cells, and bone cells using conditional and function-selective mutant mice of the GC receptor (GR), or mice with impaired GC signaling. Importantly, GCs do not only directly affect cellular functions, but also influence the cross-talk between mesenchymal and immune cells, contributing to both beneficial and adverse effects of GCs. Given the importance of endogenous GCs as stress hormones and the wide prescription of pharmaceutical GCs, an improved understanding of GC action is decisive for tackling inflammatory bone diseases, osteoporosis, and aging.}, year = {2019}, issn = {1664-3224}, DOI = {10.3389/fimmu.2019.02460}, journal = {Frontiers in immunology}, volume = {10}, pages = {2460}, keywords = {Animals; Anti-Inflammatory Agents, pharmacology; Bone and Bones, drug effects, metabolism; Cell Communication, drug effects; Disease Susceptibility; Glucocorticoids, metabolism, pharmacology; Hormones, metabolism; Humans; Immune System, cytology, immunology, metabolism; Osteitis, etiology, metabolism, pathology; Osteoarthritis, etiology, metabolism, pathology; Osteocytes, metabolism; Signal Transduction; Stress, Physiological; Stromal Cells, metabolism; arthritis; conditional knockout mice; fracture healing; glucocorticoid receptor; glucocorticoids; inflammation; osteoporosis} } @Article { BeeviTVD2019, author = {Beevi, SS. and Tangudu, NK. and Verma, VK. and Dinesh Kumar, L.}, title = {Biodrug Suppresses Breast and Colorectal Cancer in Murine Models}, year = {2019}, journal = {Methods Mol Biol.}, volume = {1974}, pages = {245-263} } @Article { Motta2019, author = {Motta, Marialetizia and Fidan, Miray and Bellacchio, Emanuele and Pantaleoni, Francesca and Schneider-Heieck, Konstantin and Coppola, Simona and Borck, Guntram and Salviati, Leonardo and Zenker, Martin and Cirstea, Ion C. and Tartaglia, Marco}, title = {Dominant Noonan syndrome-causing LZTR1 mutations specifically affect the Kelch domain substrate-recognition surface and enhance RAS-MAPK signaling.}, abstract = {Noonan syndrome (NS), the most common RASopathy, is caused by mutations affecting signaling through RAS and the MAPK cascade. Recently, genome scanning has discovered novel genes implicated in NS, whose function in RAS-MAPK signaling remains obscure, suggesting the existence of unrecognized circuits contributing to signal modulation in this pathway. Among these genes, leucine zipper-like transcriptional regulator 1 (LZTR1) encodes a functionally poorly characterized member of the BTB/POZ protein superfamily. Two classes of germline LZTR1 mutations underlie dominant and recessive forms of NS, while constitutional monoallelic, mostly inactivating, mutations in the same gene cause schwannomatosis, a cancer-prone disorder clinically distinct from NS. Here we show that dominant NS-causing LZTR1 mutations do not affect significantly protein stability and subcellular localization. We provide the first evidence that these mutations, but not the missense changes occurring as biallelic mutations in recessive NS, enhance stimulus-dependent RAS-MAPK signaling, which is triggered, at least in part, by an increased RAS protein pool. Moreover, we document that dominant NS-causing mutations do not perturb binding of LZTR1 to CUL3, a scaffold coordinating the assembly of a multimeric complex catalyzing protein ubiquitination but are predicted to affect the surface of the Kelch domain mediating substrate binding to the complex. Collectively, our data suggest a model in which LZTR1 contributes to the ubiquitinationof protein(s) functioning as positive modulator(s) of the RAS-MAPK signaling pathway. In this model, LZTR1 mutations are predicted to variably impair binding of these substrates to the multi-component ligase complex and their efficient ubiquitination and degradation, resulting in MAPK signaling upregulation.}, year = {2019}, month = {mar}, issn = {1460-2083}, DOI = {10.1093/hmg/ddy412}, journal = {Human molecular genetics}, volume = {28}, pages = {1007--1022}, keywords = {Cullin Proteins, metabolism; Humans; Kelch Repeat; Mitogen-Activated Protein Kinases, metabolism; Models, Molecular; Mutation; Noonan Syndrome, genetics, metabolism; Protein Binding; Protein Conformation; Protein Stability; Protein Transport; Signal Transduction; Transcription Factors, chemistry, genetics, metabolism; ras Proteins, metabolism} } @Article { EscoterTorres2019, author = {Escoter-Torres, Laura and Caratti, Giorgio and Mechtidou, Aikaterini and Tuckermann, Jan and Uhlenhaut, Nina Henriette and Vettorazzi, Sabine}, title = {Fighting the Fire: Mechanisms of Inflammatory Gene Regulation by the Glucocorticoid Receptor.}, abstract = {For many decades, glucocorticoids have been widely used as the gold standard treatment for inflammatory conditions. Unfortunately, their clinical use is limited by severe adverse effects such as insulin resistance, cardiometabolic diseases, muscle and skin atrophies, osteoporosis, and depression. Glucocorticoids exert their effects by binding to the Glucocorticoid Receptor (GR), a ligand-activated transcription factor which both positively, and negatively regulates gene expression. Extensive research during the past several years has uncovered novel mechanisms by which the GR activates and represses its target genes. Genome-wide studies and mouse models have provided valuable insight into the molecular mechanisms of inflammatory gene regulation by GR. This review focusses on newly identified target genes and GR co-regulators that are important for its anti-inflammatory effects in innate immune cells, as well as mutations within the GR itself that shed light on its transcriptional activity. This research progress will hopefully serve as the basis for the development of safer immune suppressants with reduced side effect profiles.}, year = {2019}, issn = {1664-3224}, DOI = {10.3389/fimmu.2019.01859}, journal = {Frontiers in immunology}, volume = {10}, pages = {1859}, keywords = {Animals; Gene Expression Regulation, drug effects, immunology; Glucocorticoids, immunology, pharmacology; Humans; Immunosuppressive Agents, immunology, pharmacology; Receptors, Glucocorticoid, immunology; gene regulation; glucocorticoid receptor; inflammation; macrophages; mouse models} } @Article { Conaway2019, author = {Conaway, H. Herschel and Henning, Petra and Lie, Antia and Tuckermann, Jan and Lerner, Ulf H.}, title = {Glucocorticoids employ the monomeric glucocorticoid receptor to potentiate vitamin D, javax.xml.bind.JAXBElement@ee08377, and parathyroid hormone-induced osteoclastogenesis.}, abstract = {Glucocorticoid (GC) therapy decreases bone mass and increases the risk of fractures. We investigated interactions between the GC dexamethasone (DEX) and the bone resorptive agents 1,25(OH) -vitamin D (D3) and parathyroid hormone (PTH) on osteoclastogenesis. We observed a synergistic potentiation of osteoclast progenitor cell differentiation and formation of osteoclasts when DEX was added to either D3- or PTH-treated mouse bone marrow cell (BMC) cultures. Cotreatment of DEX with D3 or PTH increased gene encoding calcitonin receptor ( ), acid phosphatase 5, tartrate resistant ( ), cathepsin K ( ), and TNF superfamily member 11 ( ) mRNA, receptor activator of NF-κB ligand protein (RANKL), numbers of osteoclasts on plastic, and pit formation and release of C-terminal fragment of type I collagen from cells cultured on bone slices. Enhanced RANKL protein expression caused by D3 and DEX was absent in BMC from mice in which the GC receptor (GR) was deleted in stromal cells/osteoblasts. Synergistic interactions between DEX and D3 on RANKL and osteoclast formation were present in BMC from mice with attenuated GR dimerization. These data demonstrate that the GR cooperates with D3 and PTH signaling, causing massive osteoclastogenesis, which may explain the rapid bone loss observed with high dosages of GC treatment.-Conaway, H. H., Henning, P., Lie, A., Tuckermann, J., Lerner, U. H. Glucocorticoids employ the monomeric glucocorticoid receptor to potentiate vitamin D and parathyroid hormone-induced osteoclastogenesis.}, year = {2019}, month = {dec}, issn = {1530-6860}, DOI = {10.1096/fj.201802729RRR}, journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology}, volume = {33}, pages = {14394--14409}, keywords = {Animals; Cholecalciferol, pharmacology; Dexamethasone, pharmacology; Drug Synergism; Gene Deletion; Gene Expression Regulation, drug effects; Mice; Osteogenesis, drug effects; Parathyroid Hormone, pharmacology; RANK Ligand, genetics, metabolism; Receptors, Glucocorticoid, metabolism; bone resorption; calcium-regulating hormones; osteoclasts; osteoporosis} } @Article { KalvisaSPCNSVTWMG2018, author = {Kalvisa, A. and Siersb{\ae}k, MS. and Pr{\ae}stholm, SM. and Christensen, LJL. and Nielsen, R. and Stohr, O. and Vettorazzi, S. and Tuckermann, J. and White, M. and Mandrup, S. and Gr{\o}ntved, L.}, title = {Insulin signaling and reduced glucocorticoid receptor activity attenuate postprandial gene expression in liver}, year = {2018}, month = {12}, day = {10}, journal = {PLoS Biol.}, volume = {16}, pages = {e2006249}, number = {12} } @Article { MottaFBPSCBSZCT2018, author = {Motta, M. and Fidan, M. and Bellacchio, E. and Pantaleoni, F. and Schneider-Heieck, K. and Coppola, S. and Borck, G. and Salviati, L. and Zenker, M. and Cirstea, IC. and Tartaglia, M.}, title = {Dominant Noonan syndrome-causing LZTR1 mutations specifically affect the kelch domain substrate-recognition surface and enhance RAS-MAPK signaling}, year = {2018}, month = {11}, day = {27}, journal = {Hum Mol Genet.}, volume = {28}, pages = {1007-1022}, number = {6} } @Article { KoenenCVCFBKBT2018, author = {Koenen, M. and Culemann, S. and Vettorazzi, S. and Caratti, G. and Frappart, L. and Baum, W. and Kr{\"o}nke, G. and Baschant, U. and Tuckermann, J.P.}, title = {Glucocorticoid receptor in stromal cells is essential for glucocorticoid-mediated suppression of inflammation in arthritis}, year = {2018}, month = {11}, journal = {Ann Rheum Dis.}, volume = {77}, pages = {1610-1618}, number = {11} } @Article { AramackiTEESBLAHGBLWKWGSSPZBRVWTSRWKRBHKS2018, author = {Aramacki, M. and Trugenberger, AK. and Ellwanger, AK. and Eiseler, T. and Schwerdt, C. and Bettac, L. and Langgartner, D. and Azoitei, N. and Halbgebauer, R. and Gro{\"s}, R. and Barth, T. and Lechel, A. and Walter, BM. and Kraus, JM. and Wiegreffe, C. and Grimm, J. and Scheffold, A. and Schneider, MR. and Peuker, K. and Zei{\"s}ig, S. and Britsch, S. and Rose-John, S. and Vettorazzi, S. and Wolf, E. and Tannapfel, A. and Steinestel, K. and Reber, S. and Walther, P. and Kestler, HA. and Radermacher, P. and Barth, TF. and Huber-Lang, M. and Kleger, A. and Seufferlein, T.}, title = {Thirty-eight-negative kinase 1 mediates trauma-induced intestinal injury and multi-organ failure}, year = {2018}, month = {11}, day = {1}, journal = {J Clin Invest.}, volume = {128}, pages = {5056-5072}, number = {11} } @Article { ScholtysekIBKSCPRWKSDTHFGSK2018, author = {Scholtysek, C. and Ipseiz, N. and B{\"o}hm, C. and Krishnacoumar, B. and Stenzel, M. and Czerwinski, T. and Palumbo-Zerr, K. and Rothe, T. and Weidner, D. and Klej, A. and Stoll, C. and Distler, J. and Tuckermann, J. and Herrmann, M. and Fabry, B. and Goldmann, W. and Schett, G. and Kr{\"o}nke, G.}, title = {NR4A1 regulates motility of osteoclast precursors and serves as target for the modulation of systemic bone turnover}, year = {2018}, month = {11}, journal = {J Bone Miner Res.}, volume = {33}, pages = {2035-2047}, number = {11} } @Article { AhmadKJRPT2018, author = {Ahmad, M. and Kroll, T. and Jakob, J. and Rauch, A. and Ploubidou, A. and Tuckermann, J.}, title = {Cell-based RNAi screening and high-content analysis in primary calvarian osteoblasts applied to identification of osteoblast differentiation regulators}, year = {2018}, month = {9}, day = {19}, journal = {Sci Rep.}, volume = {8}, pages = {14045}, number = {1} } @Article { PickeCBKSTWRVBSTSAHS2018, author = {Picke, AK. and Campbell, GM. and Bl{\"u}her, M. and Kr{\"u}gel, U. and Schmidt, FN. and Tsourdi, E. and Winzer, M. and Rauner, M. and Vukicevic, V. and Busse, B. and Salbach-Hirsch, J. and Tuckermann, JP. and Simon, JC. and Anderegg, U. and Hofbauer, LC. and Saalbach, A.}, title = {Thy-1 (CD90) promotes bone formation and protects against obesity}, year = {2018}, month = {8}, day = {8}, journal = {Sci Transl Med.}, volume = {10}, number = {453} } @Article { BallegeerLTEVTDSVWRTVTRIBBVL2018, author = {Ballegeer, M. and Looveren, K.V. and Timmermans, S. and Eggermont, M. and Vandevyver, S. and Thery, F. and Dendoncker, K. and Souffriau, J. and Vandewalle, J. and Wyngene, L.V. and Rycke, R. and Takahashi, N. and Vandenabeele, P. and Tuckermann, J. and Reichardt, H.M. and Impens, F. and Beyaert, R. and Bosscher, K. and Vandenbroucke, R.E. and Libert, C.}, title = {Glucocorticoid receptor dimers control intestinal STAT1 and TNF-induced inflammation in mice}, year = {2018}, month = {8}, day = {1}, journal = {J Clin Invest}, volume = {128}, pages = {3265-3279}, number = {8} } @Article { TanguduAVWLVLV2017, author = {Tangudu, NK. and Alan, B. and Vinchi, F. and W{\"o}rle, K. and Lai, D. and Vettorazzi, S. and Leopold, K. and Vuji{\c} Spasi{\c}, M.}, title = {Scavenging reactive oxygen species production normalizes ferroportin expression and ameliorates cellular and systemic iron disbalances in hemolytic mouse model}, year = {2018}, month = {8}, journal = {Antioxid Redox Signal }, volume = {29}, pages = {484-499}, number = {5} } @Article { UrbanczykSSJMM2018, author = {Urbanczyk, S. and Stein, M. and Schuh, W. and J{\"a}ck, HM. and Mougiakakos, D. and Mielenz, D.}, title = {Regulation of Energy Metabolism during Early B Lymphocyte Development}, year = {2018}, month = {7}, day = {27}, journal = {Int J Mol Sci.}, volume = {19}, number = {8} } @Article { IgnatiusT2018, author = {Ignatius, A. and Tuckermann, J.}, title = {New horizons for osteoanabolic treatment?}, year = {2018}, month = {7}, day = {26}, journal = {Nat Rev Endocrinol.}, volume = {14}, pages = {508-509}, number = {9} } @Article { DharANKGCSYVLMSTSZK2018, author = {Dhar, D. and Antonucci, L. and Nakagawa, H. and Kim, J.Y. and Glitzner, E. and Caruso, S. and Shalapour, S. and Yang, L. and Valasek, M.A. and Lee, S. and Minnich, K. and Seki, E. and Tuckermann, J. and Sibilia, M. and Zucman-Rossi, J. and Karin, M.}, title = {Liver Cancer Initiation Requires p53 Inhibition by CD44-Enhanced Growth Factor Signaling}, year = {2018}, month = {6}, day = {11}, journal = {Cancer Cell. }, volume = {33}, pages = {1061 - 1077}, number = {6} } @Article { MullerZAdLKZKHVTvdGWC2018, author = {M{\"u}ller, C. and Zidek, L.M. and Ackermann, T. and de Jong, T. and Liu, P. and Kliche, V. and Zaini, M.A. and Kortman, G. and Harkema, L. and Verbeek, D.S. and Tuckermann, J.P. and von Maltzahn, J. and de Bruin, A. and Guryev, V. and Wang, Z.Q. and Calkhoven, C.F.}, title = {Reduced expression of C/EBPβ-LIP extends health and lifespan in mice}, year = {2018}, month = {6}, day = {4}, journal = {Elife} } @Article { LinderHGZHBRTSWS2018, author = {Linder, M. and Hecking, M. and Glitzner, E. and Zwerina, K. and Holcmann, M. and Bakiri, L. and Ruocco, MG and Tuckermann, J. and Schett, G. and Wagner, EF. and Sibilia, M.}, title = {EGFR controls bone development by negatively regulating mTOR-signaling during osteoblast differentiation}, year = {2018}, month = {6}, journal = {Cell Death Differ.}, volume = {25}, pages = {1094-1106}, number = {6} } @Article { RaunerBDGHHHJKKMSTZ2018, author = {Rauner, M. and Buttgereit, F. and Distler, J. and Garbe, A.I. and Herrmann, M. and Hofbauer, L. and Hoffmann, M. and Jessberger, R. and Kornak, U. and Kr{\"o}nke, G. and Mundlos, S. and Spies, C. and Tuckermann, J. and Zwerina, J.}, title = {Osteoimmunology-IMMUNOBONE : Regulation of bone by inflammation}, year = {2018}, month = {5}, journal = {Z Rheumatol}, volume = {77}, pages = {12-15}, number = {1} } @Article { KamradtADDGIKKPPSSTW2018, author = {Kamradt, T. and Amling, M. and Dankbar, B. and Dudeck, A. and Gunzer, M. and Ignatius, A. and Kr{\"o}nke, G. and Kubatzky, K. and Pap, T. and Prinz, I. and Schett, G. and Schinke, T. and Tuckermann, J. and Waisman, A.}, title = {Mutual influence of immune system and bones}, year = {2018}, month = {5}, journal = {Z Rheumatol}, volume = {77}, pages = {8-11}, number = {1} } @Article { RappHKKTI2017, author = {Rapp, A.E. and Hachemi, Y. and Kemmler, J. and Koenen, M. and Tuckermann, J. P. and Ignatius, A.}, title = {Induced global deletion of glucocorticoid receptor impairs fracture healing}, year = {2018}, month = {4}, journal = {FASEB J. 2017}, volume = {32}, pages = {2235-2245}, number = {4} } @Article { HachemiRPWIT2018, author = {Hachemi, Y. and Rapp, A. and Picke, AK. and Weidinger, G. and Ignatius, A. and Tuckermann, J.}, title = {Molecular Mechanisms of Glucocorticoids on Skeleton and Regeneration after Fracture}, year = {2018}, month = {3}, day = {27}, journal = {J Mol Endocrinol}, volume = {61}, pages = {R75 - R90}, number = {1} } @Article { BaakeJSRBTRFR2018, author = {Baake, T. and J{\"o}r{\"s}, K. and Suennemann, J. and Ro{\"s}mann, L. and Bohnenberger, H. and Tuckermann, J.P. and Reichhardt, HM. and Fischer, HJ. and Reichardt, SD.}, title = {The glucocorticoid receptor in recipient cells keeps cytokine secretion in acute graft-versus-host disease at bay}, year = {2018}, month = {3}, day = {2}, journal = {Oncotarget}, volume = {9}, pages = {15437-15450}, number = {21} } @Article { BarteltBBKMSHOYDTAHSHN2018, author = {Bartelt, A. and Behler-Janbeck, F. and Beil, FT. and Koehne, T. and M{\"u}ller, B. and Schmidt, T. and Heine, M. and Ochs, L. and Yilmaz, T. and Dietrich, M. and Tuckermann, J.P. and Amling, M. and Herz, J. and Schinke, T. and Heeren, J. and Niemeier, A.}, title = {Lrp1 in osteoblasts controls osteoclast activity and protects against osteoporosis by limiting PDGF-RANKL signaling}, year = {2018}, month = {2}, day = {26}, journal = {Bone Res.}, volume = {6}, number = {4} } @Article { LaiTHWMTMDV2017, author = {Lai, D. and Teng, F. and Hammad, S. and Werle, J. and Maas, T. and Teufel, A. and Muckenthaler, M. U. and Dooley, S. and Vuji{\c} Spasi{\c}, M.}, title = {Hepatic Smad7-overexpression causes severe iron overload in the mouse.}, year = {2018}, month = {2}, day = {1}, journal = {Blood}, volume = {131}, pages = {581-585}, number = {5} } @Article { LeeLTJTTWHBFVBZT2017, author = {Lee, S. and Liu, P. and Teinturier, R. and Jakob, J. and Tschaffon, M. and Tasdogan, A. and Wittig, R. and Hoeller, S. and Baumhoer, D. and Frappart, L. and Vettorazzi, S. and Bertolino, P. and Zhang, C. and Tuckermann, J. P.}, title = {Deletion of Menin in craniofacial osteogenic cells in mice elicits development of mandibular ossifying fibroma}, year = {2018}, month = {2}, day = {1}, journal = {Oncogene}, volume = {37}, pages = {616-626}, number = {5} } @Article { HaffnerLuntzerKLMHLTI2018, author = {Haffner-Luntzer, M. and Kovtun, A. and Lackner, I. and M{\"o}dinger, Y. and Hacker, S. and Liedert, A. and Tuckermann, J. and Ignatius, A.}, title = {Estrogen receptor α- (ERα), but not ERβ-signaling, is crucially involved in mechanostimulation of bone fracture healing by whole-body vibration}, year = {2018}, month = {1}, day = {20}, journal = {Bone}, pages = {11-20}, number = {110} } @Article { TuSFWCTCSZ2017, author = {Tu, J. and Stoner, S. and Fromm, PD. and Wang, T. and Chen, D. and Tuckermann, J. P. and Cooper, M. S. and Seibel, MJ. and Zhou, H.}, title = {Endogenous glucocorticoid signaling in chondrocytes attenuates joint inflammation and damage.}, year = {2018}, month = {1}, journal = {FASEB J.}, volume = {32}, pages = {478-487}, number = {1} } @Article { GaluppoVHSTBF2017, author = {Galuppo, P. and Vettorazzi, S. and H{\"o}velmann, J. and Scholz, C.-J. and Tuckermann, J. P. and Bauersachs, J. and Fracarollo, D.}, title = {The glucocorticoid receptor in monocyte-derived macrophages is critical for cardiac infarct repair and remodeling}, year = {2017}, month = {11}, journal = {FASEB J.}, volume = {31}, pages = {5122-5132}, number = {11} } @Article { QuartaCZYJLYGLFBZFKKVLHBBLSGBPTHSCLSMDFT2017, author = {Quarta, C. and Clemmensen, C. and Zhu, Z. and Yang, B. and Joseph, SS. and Lutter, D. and Yi, CX. and Garc{\'i}a-C{\'a}ceres, C. and Legutko, B. and Fischer, K. and Brommage, R. and Zizzari, P. and Franklin, BS. and Krueger, M. and Koch, M. and Vettorazzi, S. and Li, P. and Hofmann, S. M. and Bakhti, M. and Bastidas-Ponce, A. and Lickert, H. and Strom, TM. and Gailus-Durner, V. and Bechmann, I. and Perez-Tilve, D. and Tuckermann, J. P. and Hrab{\v{e}} de Angelis, M. and Sandoval, D. and Cota, D. and Latz, E. and Seeley, RJ. and M{\"u}ller, T. D. and DiMarchi, RD. and Finan, B. and Tsch{\"o}p, M. H.}, title = {Molecular Integration of Incretin and Glucocorticoid Action Reverses Immunometabolic Dysfunction and Obesity}, year = {2017}, month = {10}, day = {3}, journal = {Cell Metab.}, volume = {26}, pages = {620-632}, number = {4} } @Article { HassnainWaqasNHAPSGR2017, author = {Hassnain Waqas, SF. and Noble, A. and Hoang, AC. and Ampem, G. and Popp, M. and Strau{\"s}, S. and Guille, M. and R{\"o}szer, T.}, title = {Adipose tissue macrophages develop from bone marrow-independent progenitors in Xenopus laevis and mouse}, year = {2017}, month = {9}, journal = {J Leukoc Biol.}, volume = {102}, pages = {845-855}, number = {3}, keywords = {CX3CR1; fat body; neuropeptide FF; yolk sac M{\\&}#981;s} } @Article { SteinDMBFRUSSBWJM2017, author = {Stein, M. and D{\"u}tting, S. and Mougiakakos, D. and B{\"o}sl, M. and Fritsch, K. and Reimer, D. and Urbanczyk, S. and Steinmetz, T. and Schuh, W. and Bozec, A. and Winkler, TH. and J{\"a}ck, H. M. and Mielenz, D.}, title = {A defined metabolic state in pre B cells governs B-cell development and is counterbalanced by Swiprosin-2/EFhd1}, year = {2017}, month = {7}, journal = {Cell Death Differ.}, volume = {24}, pages = {1239-1252}, number = {7} } @Article { PantaleoniLCMLBCLPFNCAST2017, author = {Pantaleoni, F. and Lev, D. and Cirstea, IC. and Motta, M. and Lepri, FR. and Bottero, L. and Cecchetti, S. and Linger, I. and Paolacci, S. and Flex, E. and Novelli, A. and Care, A. and Ahmadian, MR. and Stellacci, E. and Tartaglia, M.}, title = {Aberrant HRAS transcript processing underlies a distinctive phenotype within the RASopathy clinical spectrum}, year = {2017}, month = {7}, journal = {Hum Mutat. }, volume = {38}, pages = {798-804}, number = {7} } @Article { WaqasHLAABTCGNLMRPQASSBLSR2017, author = {Waqas, SFH. and Hoang, AC. and Lyn, JT. and Ampem, G. and Azegrouz, H. and Balogh, L. and Thuroczy, J. and Chen, JC. and Gerling, IC. and Nam, S. and Lim, JS. and Martinez-Iba{\~n}ez, J. and Real, JT. and Paschke, S. and Quillet, R. and Ayachi, S. and Simonin, F. and Schneider, EM. and Brinkman, JA. and Lamming, DW. and Seroogy, CM. and R{\"o}szer, T.}, title = {Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages}, year = {2017}, month = {6}, day = {30}, journal = {J Clin Invest.}, volume = {127}, pages = {2842-2854}, number = {7} } @Article { WittigBlaichWSLBGSMLJCHSBM2017, author = {Wittig-Blaich, S. and Wittig, R. and Schmidt, S. and Lyer, S. and Bewerunge-Hudler, M. and Gronert-Sum, S. and Strobel-Freidekind, O. and M{\"u}ller, C. and List, M. and Jaskot, A. and Christiansen, H. and Hafner, M. and Schadendorf, D. and Block, I. and Mollenhauer, J.}, title = {Systematic screening of isogenic cancer cells identifies DUSP6 as context-specific synthetic lethal target in melanoma.}, year = {2017}, month = {4}, day = {4}, journal = {Oncotarget}, volume = {8}, pages = {23760-23774}, number = {14} } @Article { LiuLKROLMLZNWRDBZT2017, author = {Liu, P. and Lee, S. and Knoll, J. and Rauch, A. and Ostermay, S. and Luther, J. and Malkusch, N. and Lerner, U. H. and Zaiss, MM. and Neven, M. and Wittig, R. and Rauner, M. and David, J. P. and Bertolino, P. and Zhang, CX. and Tuckermann, J. P.}, title = {Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis.}, year = {2017}, month = {4}, journal = {Cell Death Differ.}, volume = {24}, pages = {672-682}, number = {4} } @Article { MuellerHKVBMAJFEMTMHSBTM2016, author = {Mueller, KM and Hartmann, K. and Kaltenecker, D and Vettorazzi, S. and Bauer, M. and Mauser, L. and Amann, S and Jall, S. and Fischer, K. and Esterbauer, H. and M{\"u}ller, T. D. and Tsch{\"o}p, M. H. and Magnes, C and Haybaeck, J. and Scherer, T and Bordag, N and Tuckermann, J. P. and Moriggi, R.}, title = {Adipocyte Glucocorticoid Receptor Deficiency Attenuates Aging- and Hfd-Induced Obesity, and Impairs the Feeding-Fasting Transition.}, year = {2017}, month = {2}, journal = {Diabetes}, volume = {66}, pages = {272-286}, number = {2} } @Article { Roszer2016, author = {R{\"o}szer, T.}, title = {Transcriptional control of apoptotic cell clearance by macrophage nuclear receptors.}, year = {2017}, month = {2}, journal = {Apoptosis}, volume = {22}, pages = {284-294}, number = {2} } @Article { TanguduV2017, author = {Tangudu, Naveen Kumar and Vuji{\c} Spasi{\c}, M.}, title = {Heme Activates Macrophage Hepcidin Expression via Toll like Receptor 4 and Extracellular Signal-Regulated Kinases Signaling Pathway}, year = {2017}, month = {1}, day = {21}, journal = {Clinical Pharmacology {\\&} Biopharmaceutics}, volume = {6}, pages = {166} } @Article { KlasenKDVVLMTBLR2017, author = {Kla{\"s}en, C. and Karabinskaya, A. and Dejager, L. and Vettorazzi, S. and Van Moorleghem, J. and Luhder, F. and Meijsing, S.H. and Tuckermann, J. P. and Bohnenberger, H. and Libert, C. and Reichardt, H.M.}, title = {Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma}, year = {2017}, month = {1}, day = {17}, journal = {J Immunol. }, volume = {199}, pages = {48-61}, number = {1} } @Article { LunovaSNLKSVHRJDVTS2017, author = {Lunova, M. and Schwarz, P. and Nuraldeen, R. and Levada, K. and Kuscuoglu, D. and St{\"u}tzle, M. and Vuji{\c} Spasi{\c}, M. and Haybaeck, J. and Ruchala, P. and Jirsa, M. and Deschemin, JC. and Vaulont, S. and Trautwein, C. and Strnad, P.}, title = {Hepcidin knockout mice spontaneously develop chronic pancreatitis owing to cytoplasmic iron overload in acinar cells.}, year = {2017}, month = {1}, journal = {J Pathol.}, volume = {241}, pages = {104-114}, number = {1} } @Article { Pantaleoni2017, author = {Pantaleoni, Francesca and Lev, Dorit and Cirstea, Ion C. and Motta, Marialetizia and Lepri, Francesca Romana and Bottero, Lisabianca and Cecchetti, Serena and Linger, Ilan and Paolacci, Stefano and Flex, Elisabetta and Novelli, Antonio and Car{\`e}, Alessandra and Ahmadian, Mohammad R. and Stellacci, Emilia and Tartaglia, Marco}, title = {Aberrant HRAS transcript processing underlies a distinctive phenotype within the RASopathy clinical spectrum.}, abstract = {RASopathies are a group of rare, clinically related conditions affecting development and growth, and are caused by germline mutations in genes encoding signal transducers and modulators with a role in the RAS signaling network. These disorders share facial dysmorphia, short stature, variable cognitive deficits, skeletal and cardiac defects, and a variable predisposition to malignancies. Here, we report on a de novo 10-nucleotide-long deletion in HRAS (c.481_490delGGGACCCTCT, NM_176795.4; p.Leu163ProfsTer52, NP_789765.1) affecting transcript processing as a novel event underlying a RASopathy characterized by developmental delay, intellectual disability and autistic features, distinctive coarse facies, reduced growth, and ectodermal anomalies. Molecular and biochemical studies demonstrated that the deletion promotes constitutive retention of exon IDX, which is generally skipped during HRAS transcript processing, and results in a stable and mildly hyperactive GDP/GTP-bound protein that is constitutively targeted to the plasma membrane. Our findings document a new mechanism leading to altered HRAS function that underlies a previously unappreciated phenotype within the RASopathy spectrum.}, year = {2017}, month = {jul}, issn = {1098-1004}, DOI = {10.1002/humu.23224}, journal = {Human mutation}, volume = {38}, pages = {798--804}, keywords = {Animals; Autistic Disorder, genetics; COS Cells; Cell Membrane, metabolism; Child; Child, Preschool; Chlorocebus aethiops; Developmental Disabilities, genetics; Exons; Facies; Gene Deletion; Gene Expression Regulation, Neoplastic; Genes, ras; Germ-Line Mutation; Humans; Intellectual Disability, genetics; Male; Phenotype; Proto-Oncogene Proteins p21(ras), genetics; RNA, Messenger, metabolism; Signal Transduction; Costello syndrome; HRAS; RAS signaling; RASopathies; transcript processing} } @Article { pmid27596806, author = {Conaway, H. H. and Henning, P. and Lie, A. and Tuckermann, J. P. and Lerner, U. H.}, title = {Activation of dimeric glucocorticoid receptors in osteoclast progenitors potentiates RANKL induced mature osteoclast bone resorbing activity}, year = {2016}, month = {12}, journal = {Bone}, volume = {93}, pages = {43-54} } @Article { BarcalaTabarrozziADCGABALVTDP2016, author = {Barcala Tabarrozzi, AE. and Andreone, L. and Deckers, J. and Castro, CN. and Gimeno, ML. and Ariolfo, L. and Berguer, PM. and Antunica-Noguerol, M. and Libermann, AC. and Vettorazzi, S. and Tuckermann, J. P. and De Bosscher, K. and Perone, MJ}, title = {GR-independent down-modulation on GM-CSF bone marrow-derived dendritic cells by the selective glucocorticoid receptor modulator Compound A.}, year = {2016}, month = {11}, day = {18}, journal = {Sci Rep.}, volume = {6}, pages = {36646} } @Article { JavaheriKPPKNSNSMHAWTLHTKMDURGKM2016, author = {Javaheri, T. and Kazemi, Z. and Pencik, J and Pham, HT and Kauer, M. and Noorizadeh, R and Sax, B and Nivarthi, H and Schlederer, M and Maurer, B. and Hofbauer, M and Aryee, DN and Wiedner, M and Tomazou, EM and Logan, M and Hartmann, C. and Tuckermann, J. P. and Kenner, L. and Mikula, M and Dolznig, H. and {\"U}ren, A and Richter, GH and Grebien, F and Kovar, H. and Moriggl, R.}, title = {Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation}, year = {2016}, month = {10}, day = {13}, journal = {Cell Death Dis.}, volume = {7}, pages = {e2419}, number = {10} } @Article { pmid27720451, author = {Finan, B. and Clemmensen, C. and Zhu, Z. and Stemmer, K. and Gauthier, K. and M{\"u}ller, L. and De Angelis, M. and Moreth, K. and Neff, F. and Perez-Tilve, D. and Fischer, K. and Lutter, D. and Sanchez-Garrido, M. A. and Liu, P. and Tuckermann, J. P. and Malehmir, M. and Healy, M. E. and Weber, A. and Heikenwalder, M. and Jastroch, M. and Kleinert, M. and Jall, S. and Brandt, S. and Flamant, F. and Schramm, K. W. and Biebermann, H. and Doring, Y. and Weber, C. and Habegger, K. M. and Keuper, M. and Gelfanov, V. and Liu, F. and K{\"o}hrle, J. and Rozman, J. and Fuchs, H. and Gailus-Durner, V. and Hrab{\v{e}} de Angelis, M. and Hofmann, S. M. and Yang, B. and Tsch{\"o}p, M. H. and DiMarchi, R. and M{\"u}ller, T. D.}, title = {Chemical Hybridization of Glucagon and Thyroid Hormone Optimizes Therapeutic Impact for Metabolic Disease}, year = {2016}, month = {10}, day = {5}, journal = {Cell}, volume = {167}, pages = {843-857}, number = {3} } @Article { pmid27554624, author = {Liu, P. and Baumgart, M. and Groth, M. and Wittmann, J. and J{\"a}ck, H. M. and Platzer, M. and Tuckermann, J. P. and Baschant, U.}, title = {Dicer ablation in osteoblasts by Runx2 driven cre-loxP recombination affects bone integrity, but not glucocorticoid-induced suppression of bone formation}, year = {2016}, month = {8}, day = {24}, journal = {Sci Rep}, volume = {6}, pages = {32112} } @Article { pmid27367288, author = {Kroll, T. and Schmidt, D. and Schwanitz, G. and Ahmad, M. and Hamann, J. and Schlosser, C. and Lin, Y. C. and B{\"o}hm, K. J. and Tuckermann, J. P. and Ploubidou, A.}, title = {High-Content Microscopy Analysis of Subcellular Structures:Assay Development and Application to Focal Adhesion Quantification}, year = {2016}, month = {7}, day = {1}, journal = {Curr Protoc Cytom}, volume = {77}, pages = {1-12} } @Article { pmid27129231, author = {Chen, S. and Feng, T. and Vuji{\c} Spasi{\c}, M. and Altamura, S. and Breitkopf-Heinlein, K. and Altenoder, J. and Weiss, T. S. and Dooley, S. and Muckenthaler, M. U.}, title = {Transforming Growth Factor β1 (TGF-β1) Activates Hepcidin mRNA Expression in Hepatocytes}, year = {2016}, month = {6}, day = {17}, journal = {J. Biol. Chem.}, volume = {291}, pages = {13160-13174}, number = {25} } @Article { pmid27191748, author = {Minas, T. Z. and Surdez, D. and Javaheri, T. and Tanaka, M. and Howarth, M. and Kang, H. J. and Han, J. and Han, Z. Y. and Sax, B. and Kream, B. E. and Hong, S. H. and Celik, H. and Tirode, F. and Tuckermann, J. P. and Toretsky, J. A. and Kenner, L. and Kovar, H. and Lee, S. and Sweet-Cordero, E. A. and Nakamura, T. and Moriggl, R. and Delattre, O. and Uren, A.}, title = {Combined experience of six independent laboratories attempting to create an Ewing sarcoma mouse model}, year = {2016}, month = {5}, day = {15}, journal = {Oncotarget}, volume = {23}, pages = {34141-34163}, number = {8} } @Article { pmid26639395, author = {Robert, O. and Boujedidi, H. and Bigorgne, A. and Ferrere, G. and Voican, C. S. and Vettorazzi, S. and Tuckermann, J. P. and Bouchet-Delbos, L. and Tran, T. and Hemon, P. and Puchois, V. and Dagher, I. and Douard, R. and Gaudin, F. and Gary-Gouy, H. and Capel, F. and Durand-Gasselin, I. and Prevot, S. and Rousset, S. and Naveau, S. and Godot, V. and Emilie, D. and Lombes, M. and Perlemuter, G. and Cassard, A. M.}, title = {Decreased expression of the glucocorticoid receptor-GILZ pathway in Kupffer cells promotes liver inflammation in obese mice}, year = {2016}, month = {4}, journal = {J. Hepatol.}, volume = {S0168-8278}, pages = {781-783}, number = {15} } @Article { pmid26842265, author = {Hartmann, K. and Koenen, M. and Schauer, S. and Wittig-Blaich, S. and Ahmad, M. and Baschant, U. and Tuckermann, J. P.}, title = {Molecular Actions of Glucocorticoids in Cartilage and Bone During Health, Disease, and Steroid Therapy}, year = {2016}, month = {4}, journal = {Physiol. Rev.}, volume = {96}, pages = {409-447}, number = {2} } @Article { pmid26239911, author = {Ampem, G. and Azegrouz, H. and Bacsadi, A. and Balogh, L. and Schmidt, S. and Thuroczy, J. and R{\"o}szer, T.}, title = {Adipose tissue macrophages in non-rodent mammals: a comparative study}, year = {2016}, month = {2}, journal = {Cell Tissue Res.}, volume = {363}, pages = {461-478}, number = {2} } @Article { pmid26672929, author = {Asfar, P. and Russell, JA and Tuckermann, J. P. and Radermacher, P.}, title = {Selepressin in Septic Shock: A Step Toward Decatecholaminization?}, year = {2016}, month = {1}, journal = {Crit Care Med.}, volume = {44}, pages = {234-236}, number = {1} } @Article { pmid25910399, author = {H{\"u}bner, S. and Dejager, L. and Libert, C. and Tuckermann, J. P.}, title = {The glucocorticoid receptor in inflammatory processes: transrepression is not enough}, year = {2015}, month = {11}, journal = {Biol. Chem.}, volume = {396}, pages = {1223-1231}, number = {11} } @Article { pmid26183376, author = {Vettorazzi, S. and Bode, C. and Dejager, L. and Frappart, L. and Shelest, E. and Klassen, C. and Tasdogan, A. and Reichardt, H. M. and Libert, C. and Schneider, M. and Weih, F. and Henriette Uhlenhaut, N. and David, J. P. and Graler, M. and Kleiman, A. and Tuckermann, J. P.}, title = {Glucocorticoids limit acute lung inflammation in concert with inflammatory stimuli by induction of SphK1}, year = {2015}, month = {7}, day = {17}, journal = {Nat Commun}, volume = {6}, pages = {7796} } @Article { pmid25733567, author = {Talaber, G. and Tuckermann, J. P. and Okret, S.}, title = {ACTH controls thymocyte homeostasis independent of glucocorticoids}, year = {2015}, month = {6}, journal = {FASEB J.}, volume = {29}, pages = {2526-2534}, number = {6} } @Article { pmid25957148, author = {Lim, H. W. and Uhlenhaut, N. H. and Rauch, A. and Weiner, J. and H{\"u}bner, S. and Hubner, N. and Won, K. J. and Lazar, M. A. and Tuckermann, J. P. and Steger, D. J.}, title = {Genomic redistribution of GR monomers and dimers mediates transcriptional response to exogenous glucocorticoid in vivo}, year = {2015}, month = {6}, journal = {Genome Res.}, volume = {25}, pages = {836-844}, number = {6} } @Article { pmid26089604, author = {R{\"o}szer, T.}, title = {Understanding the Mysterious M2 Macrophage through Activation Markers and Effector Mechanisms}, year = {2015}, month = {5}, journal = {Mediators Inflamm.}, volume = {2015}, pages = {816460} } @Article { pmid25847991, author = {Matthews, L. C. and Berry, A. A. and Morgan, D. J. and Poolman, T. M. and Bauer, K. and Kramer, F. and Spiller, D. G. and Richardson, R. V. and Chapman, K. E. and Farrow, S. N. and Norman, M. R. and Williamson, A. J. and Whetton, A. D. and Taylor, S. S. and Tuckermann, J. P. and White, M. R. and Ray, D. W.}, title = {Glucocorticoid receptor regulates accurate chromosome segregation and is associated with malignancy}, year = {2015}, month = {4}, day = {28}, journal = {Proc. Natl. Acad. Sci. U.S.A.}, volume = {112}, pages = {5479-5484}, number = {17} } @Article { pmid25510234, author = {Schubert, N. and Dudeck, J. and Liu, P. and Karutz, A. and Speier, S. and Maurer, M. and Tuckermann, J. P. and Dudeck, A.}, title = {Mast cell promotion of T cell-driven antigen-induced arthritis despite being dispensable for antibody-induced arthritis in which T cells are bypassed}, year = {2015}, month = {4}, journal = {Arthritis Rheumatol}, volume = {67}, pages = {903-913}, number = {4} } @Article { pmid25358639, author = {Theiss-Suennemann, J. and Jorss, K. and Messmann, J. J. and Reichardt, S. D. and Montes-Cobos, E. and Luhder, F. and Tuckermann, J. P. and Wolff, H. and Dressel, R. and Grone, H. J. and Strauss, G. and Reichardt, H. M.}, title = {Glucocorticoids attenuate acute graft-versus-host disease by suppressing the cytotoxic capacity of CD8(+) T cells}, year = {2015}, month = {3}, journal = {J. Pathol.}, volume = {235}, pages = {646-655}, number = {4} } @Article { pmid25574839, author = {Menendez-Gutierrez, M. P. and R{\"o}szer, T. and Fuentes, L. and Nunez, V. and Escolano, A. and Redondo, J. M. and De Clerck, N. and Metzger, D. and Valledor, A. F. and Ricote, M.}, title = {Retinoid X receptors orchestrate osteoclast differentiation and postnatal bone remodeling}, year = {2015}, month = {2}, journal = {J. Clin. Invest.}, volume = {125}, pages = {809-823}, number = {2} } @Article { pmid26215995, author = {Frenkel, B. and White, W. and Tuckermann, J. P.}, title = {Glucocorticoid-Induced Osteoporosis}, year = {2015}, journal = {Adv. Exp. Med. Biol.}, volume = {872}, pages = {179-215} } @Article { pmid25333229, author = {Nivarthi, H. and Prchal-Murphy, M. and Swoboda, A. and Hager, M. and Schlederer, M. and Kenner, L. and Tuckermann, J. P. and Sexl, V. and Moriggl, R. and Ermakova, O.}, title = {Stat5 gene dosage in T cells modulates CD8+ T-cell homeostasis and attenuates contact hypersensitivity response in mice}, year = {2015}, month = {1}, journal = {Allergy}, volume = {70}, pages = {67-79}, number = {1} } @Article { NakhaeiRad2015, author = {Nakhaei-Rad, Saeideh and Nakhaeizadeh, Hossein and Kordes, Claus and Cirstea, Ion C. and Schmick, Malte and Dvorsky, Radovan and Bastiaens, Philippe I. H. and H{\"a}ussinger, Dieter and Ahmadian, Mohammad Reza}, title = {The Function of Embryonic Stem Cell-expressed RAS (E-RAS), a Unique RAS Family Member, Correlates with Its Additional Motifs and Its Structural Properties.}, abstract = {E-RAS is a member of the RAS family specifically expressed in embryonic stem cells, gastric tumors, and hepatic stellate cells. Unlike classical RAS isoforms (H-, N-, and K-RAS4B), E-RAS has, in addition to striking and remarkable sequence deviations, an extended 38-amino acid-long unique N-terminal region with still unknown functions. We investigated the molecular mechanism of E-RAS regulation and function with respect to its sequence and structural features. We found that N-terminal extension of E-RAS is important for E-RAS signaling activity. E-RAS protein most remarkably revealed a different mode of effector interaction as compared with H-RAS, which correlates with deviations in the effector-binding site of E-RAS. Of all these residues, tryptophan 79 (arginine 41 in H-RAS), in the interswitch region, modulates the effector selectivity of RAS proteins from H-RAS to E-RAS features.}, year = {2015}, month = {jun}, issn = {1083-351X}, DOI = {10.1074/jbc.M115.640607}, journal = {The Journal of biological chemistry}, volume = {290}, pages = {15892--15903}, keywords = {Amino Acid Motifs; Animals; COS Cells; Chlorocebus aethiops; Dogs; Humans; Madin Darby Canine Kidney Cells; Oncogene Protein p21(ras), genetics, metabolism; Protein Structure, Tertiary; Proto-Oncogene Proteins p21(ras), genetics, metabolism; Sequence Homology, Amino Acid; Signal Transduction, physiology; E-RAS; H-RAS; RAS protein; Raf kinase; effector selection; embryonic stem cell-expressed RAS; phosphatidylinositide 3-kinase (PI 3-kinase); phosphatidylinositol kinase (PI kinase); small GTPase; specificity determining residues} } @Article { pmid25940089, author = {Nakhaei-Rad, S. and Nakhaeizadeh, H. and Kordes, C. and Cirstea, I. C. and Schmick, M. and Dvorsky, R. and Bastiaens, P. I. and Haussinger, D. and Ahmadian, M. R.}, title = {The Function of Embryonic Stem Cell-expressed RAS ERAS, a Unique RAS Family Member, Correlates with I Additional Motifs and Its Structural Properties}, year = {2015}, journal = {J. Biol. Chem.}, volume = {290}, pages = {15892-15903}, number = {25} } @Article { pmid25193158, author = {Tu, J. and Henneicke, H. and Zhang, Y. and Stoner, S. and Cheng, T. L. and Schindeler, A. and Chen, D. and Tuckermann, J. P. and Cooper, M. S. and Seibel, M. J. and Zhou, H.}, title = {Disruption of glucocorticoid signaling in chondrocytes delays metaphyseal fracture healing but does not affect normal cartilage and bone development}, year = {2014}, month = {12}, journal = {Bone}, volume = {69}, pages = {12-22} } @Article { pmid25174684, author = {R{\"o}szer, T.}, title = {The invertebrate midintestinal gland ('hepatopancreas') is an evolutionary forerunner in the integration of immunity and metabolism}, year = {2014}, month = {12}, journal = {Cell Tissue Res.}, volume = {358}, pages = {685-695}, number = {3} } @Article { pmid25096715, author = {R{\"o}szer, T. and Kiss-Toth, E. D.}, title = {FMRF-amide is a glucose-lowering hormone in the snail Helix aspersa}, year = {2014}, month = {11}, journal = {Cell Tissue Res.}, volume = {358}, pages = {371-383}, number = {2} } @Article { pmid25306233, author = {Henning, P. and Liu, X. and Nagano, K. and Saito, H. and Borjesson, A. E. and Sjogren, K. and Windahl, S. H. and Farman, H. and Kindlund, B. and Engdahl, C. and Koskela, A. and Zhang, F. P. and Eriksson, E. E. and Zaman, F. and Hammarstedt, A. and Isaksson, H. and Bally, M. and Kassem, A. and Lindholm, C. and Sandberg, O. and Aspenberg, P. and Savendahl, L. and Feng, J. Q. and Tuckermann, J. P. and Tuukkanen, J. and Poutanen, M. and Baron, R. and Lerner, U. H. and Gori, F. and Ohlsson, C.}, title = {Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures}, year = {2014}, month = {11}, journal = {Nat. Med.}, volume = {20}, pages = {1279-1288}, number = {11} } @Article { pmid25057793, author = {Reichardt, S. D. and Weinhage, T. and Rotte, A. and Foller, M. and Oppermann, M. and Luhder, F. and Tuckermann, J. P. and Lang, F. and van den Brandt, J. and Reichardt, H. M.}, title = {Glucocorticoids induce gastroparesis in mice through depletion of l-arginine}, year = {2014}, month = {10}, journal = {Endocrinology}, volume = {155}, pages = {3899-3908}, number = {10} } @Article { pmid24965772, author = {Weitnauer, M. and Schmidt, L. and Ng Kuet Leong, N. and Muenchau, S. and Lasitschka, F. and Eckstein, V. and H{\"u}bner, S. and Tuckermann, J. P. and Dalpke, A. H.}, title = {Bronchial epithelial cells induce alternatively activated dendritic cells dependent on glucocorticoid receptor signaling}, year = {2014}, month = {8}, day = {1}, journal = {J. Immunol.}, volume = {193}, pages = {1475-1484}, number = {3} } @Article { pmid24862220, author = {Zhao, B. and Choi, J. P. and Jaehne, M. and Gao, Y. R. and Desai, R. and Tuckermann, J. P. and Zhou, H. and Handelsman, D. J. and Simanainen, U.}, title = {Glucocorticoid receptor in prostate epithelia is not required for corticosteroid-induced epithelial hyperproliferation in the mouse prostate}, year = {2014}, month = {7}, journal = {Prostate}, volume = {74}, pages = {1068-1078}, number = {10} } @Article { pmid24836782, author = {Asfar, P. and Tuckermann, J. P. and Radermacher, P.}, title = {Steroids and vasopressin in septic shock-brother and sister or just distant cousins?}, year = {2014}, month = {6}, journal = {Crit. Care Med.}, volume = {42}, pages = {1531-1532}, number = {6} } @Book { Roszer2014_2, author = {R{\"o}szer, T.}, title = {Nitric Oxide in Plants: Metabolism and Role in Stress Physiology}, year = {2014}, month = {5}, day = {27}, isbn = {978-3-319-06709-4}, publisher = {Springer International Publishing}, editor = {M. Nasir Khan Mohammad Mobin Firoz Mohammad Francisco J. Corpas} } @Book { Roszer2014, author = {R{\"o}szer, T.}, title = {Nitric Oxide Signaling and Nitrosative Stress in the Musculoskeletal System}, year = {2014}, month = {5}, day = {3}, isbn = {978-3-642-30017-2}, publisher = {Springer Berlin Heidelberg}, editor = {Ismail Laher} } @Article { pmid24488308, author = {Schweingruber, N. and Fischer, H. J. and Fischer, L. and van den Brandt, J. and Karabinskaya, A. and Labi, V. and Villunger, A. and Kretzschmar, B. and Huppke, P. and Simons, M. and Tuckermann, J. P. and Flugel, A. and Luhder, F. and Reichardt, H. M.}, title = {Chemokine-mediated redirection of T cells constitutes a critical mechanism of glucocorticoid therapy in autoimmune CNS responses}, year = {2014}, month = {5}, journal = {Acta Neuropathol.}, volume = {127}, pages = {713-729}, number = {5} } @Article { pmid24343796, author = {R{\"o}szer, T. and Jozsa, T. and Kiss-Toth, E. D. and De Clerck, N. and Balogh, L.}, title = {Leptin receptor deficient diabetic (db/db) mice are compromised in postnatal bone regeneration}, year = {2014}, month = {4}, journal = {Cell Tissue Res.}, volume = {356}, pages = {195-206}, number = {1} } @Article { pmid24653703, author = {Vuji{\c} Spasi{\c}, M.}, title = {Molecular basis of HFE-hemochromatosis}, year = {2014}, month = {3}, day = {11}, journal = {Front Pharmacol}, volume = {5}, pages = {42} } @Article { pmid24705357, author = {Flex, E. and Jaiswal, M. and Pantaleoni, F. and Martinelli, S. and Strullu, M. and Fansa, E. K. and Caye, A. and De Luca, A. and Lepri, F. and Dvorsky, R. and Pannone, L. and Paolacci, S. and Zhang, S. C. and Fodale, V. and Bocchinfuso, G. and Rossi, C. and Burkitt-Wright, E. M. and Farrotti, A. and Stellacci, E. and Cecchetti, S. and Ferese, R. and Bottero, L. and Castro, S. and Fenneteau, O. and Brethon, B. and Sanchez, M. and Roberts, A. E. and Yntema, H. 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