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Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor.

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Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor. / Rauch, Alexander; Seitz, Sebastian; Baschant, Ulrike; Schilling, Arndt; Illing, Anett; Stride, Brenda; Kirilov, Milen; Mandic, Vice; Takacz, Andrea; Schmidt-Ullrich, Ruth; Ostermay, Susanne; Schinke, Thorsten; Spanbroek, Rainer; Zaiss, Mario M; Angel, Peter E; Lerner, Ulf H; David, Jean-Pierre; Reichardt, Holger M; Amling, Michael; Schütz, Günther; Tuckermann, Jan P.

In: CELL METAB, Vol. 11, No. 6, 6, 2010, p. 517-531.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Rauch, A, Seitz, S, Baschant, U, Schilling, A, Illing, A, Stride, B, Kirilov, M, Mandic, V, Takacz, A, Schmidt-Ullrich, R, Ostermay, S, Schinke, T, Spanbroek, R, Zaiss, MM, Angel, PE, Lerner, UH, David, J-P, Reichardt, HM, Amling, M, Schütz, G & Tuckermann, JP 2010, 'Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor.', CELL METAB, vol. 11, no. 6, 6, pp. 517-531. <http://www.ncbi.nlm.nih.gov/pubmed/20519123?dopt=Citation>

APA

Rauch, A., Seitz, S., Baschant, U., Schilling, A., Illing, A., Stride, B., Kirilov, M., Mandic, V., Takacz, A., Schmidt-Ullrich, R., Ostermay, S., Schinke, T., Spanbroek, R., Zaiss, M. M., Angel, P. E., Lerner, U. H., David, J-P., Reichardt, H. M., Amling, M., ... Tuckermann, J. P. (2010). Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor. CELL METAB, 11(6), 517-531. [6]. http://www.ncbi.nlm.nih.gov/pubmed/20519123?dopt=Citation

Vancouver

Rauch A, Seitz S, Baschant U, Schilling A, Illing A, Stride B et al. Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor. CELL METAB. 2010;11(6):517-531. 6.

Bibtex

@article{cf5fa558b9184f3d91b36a7616a90ff4,
title = "Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor.",
abstract = "Development of osteoporosis severely complicates long-term glucocorticoid (GC) therapy. Using a Cre-transgenic mouse line, we now demonstrate that GCs are unable to repress bone formation in the absence of glucocorticoid receptor (GR) expression in osteoblasts as they become refractory to hormone-induced apoptosis, inhibition of proliferation, and differentiation. In contrast, GC treatment still reduces bone formation in mice carrying a mutation that only disrupts GR dimerization, resulting in bone loss in vivo, enhanced apoptosis, and suppressed differentiation in vitro. The inhibitory GC effects on osteoblasts can be explained by a mechanism involving suppression of cytokines, such as interleukin 11, via interaction of the monomeric GR with AP-1, but not NF-kappaB. Thus, GCs inhibit cytokines independent of GR dimerization and thereby attenuate osteoblast differentiation, which accounts, in part, for bone loss during GC therapy.",
keywords = "Animals, Mice, Mice, Knockout, Apoptosis, Cell Differentiation, Osteogenesis drug effects, Osteoblasts cytology, Dimerization, Glucocorticoids toxicity, Interleukin-11 metabolism, Receptors, Glucocorticoid genetics, Transcription Factor AP-1 metabolism, Animals, Mice, Mice, Knockout, Apoptosis, Cell Differentiation, Osteogenesis drug effects, Osteoblasts cytology, Dimerization, Glucocorticoids toxicity, Interleukin-11 metabolism, Receptors, Glucocorticoid genetics, Transcription Factor AP-1 metabolism",
author = "Alexander Rauch and Sebastian Seitz and Ulrike Baschant and Arndt Schilling and Anett Illing and Brenda Stride and Milen Kirilov and Vice Mandic and Andrea Takacz and Ruth Schmidt-Ullrich and Susanne Ostermay and Thorsten Schinke and Rainer Spanbroek and Zaiss, {Mario M} and Angel, {Peter E} and Lerner, {Ulf H} and Jean-Pierre David and Reichardt, {Holger M} and Michael Amling and G{\"u}nther Sch{\"u}tz and Tuckermann, {Jan P}",
year = "2010",
language = "Deutsch",
volume = "11",
pages = "517--531",
journal = "CELL METAB",
issn = "1550-4131",
publisher = "Cell Press",
number = "6",

}

RIS

TY - JOUR

T1 - Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor.

AU - Rauch, Alexander

AU - Seitz, Sebastian

AU - Baschant, Ulrike

AU - Schilling, Arndt

AU - Illing, Anett

AU - Stride, Brenda

AU - Kirilov, Milen

AU - Mandic, Vice

AU - Takacz, Andrea

AU - Schmidt-Ullrich, Ruth

AU - Ostermay, Susanne

AU - Schinke, Thorsten

AU - Spanbroek, Rainer

AU - Zaiss, Mario M

AU - Angel, Peter E

AU - Lerner, Ulf H

AU - David, Jean-Pierre

AU - Reichardt, Holger M

AU - Amling, Michael

AU - Schütz, Günther

AU - Tuckermann, Jan P

PY - 2010

Y1 - 2010

N2 - Development of osteoporosis severely complicates long-term glucocorticoid (GC) therapy. Using a Cre-transgenic mouse line, we now demonstrate that GCs are unable to repress bone formation in the absence of glucocorticoid receptor (GR) expression in osteoblasts as they become refractory to hormone-induced apoptosis, inhibition of proliferation, and differentiation. In contrast, GC treatment still reduces bone formation in mice carrying a mutation that only disrupts GR dimerization, resulting in bone loss in vivo, enhanced apoptosis, and suppressed differentiation in vitro. The inhibitory GC effects on osteoblasts can be explained by a mechanism involving suppression of cytokines, such as interleukin 11, via interaction of the monomeric GR with AP-1, but not NF-kappaB. Thus, GCs inhibit cytokines independent of GR dimerization and thereby attenuate osteoblast differentiation, which accounts, in part, for bone loss during GC therapy.

AB - Development of osteoporosis severely complicates long-term glucocorticoid (GC) therapy. Using a Cre-transgenic mouse line, we now demonstrate that GCs are unable to repress bone formation in the absence of glucocorticoid receptor (GR) expression in osteoblasts as they become refractory to hormone-induced apoptosis, inhibition of proliferation, and differentiation. In contrast, GC treatment still reduces bone formation in mice carrying a mutation that only disrupts GR dimerization, resulting in bone loss in vivo, enhanced apoptosis, and suppressed differentiation in vitro. The inhibitory GC effects on osteoblasts can be explained by a mechanism involving suppression of cytokines, such as interleukin 11, via interaction of the monomeric GR with AP-1, but not NF-kappaB. Thus, GCs inhibit cytokines independent of GR dimerization and thereby attenuate osteoblast differentiation, which accounts, in part, for bone loss during GC therapy.

KW - Animals

KW - Mice

KW - Mice, Knockout

KW - Apoptosis

KW - Cell Differentiation

KW - Osteogenesis drug effects

KW - Osteoblasts cytology

KW - Dimerization

KW - Glucocorticoids toxicity

KW - Interleukin-11 metabolism

KW - Receptors, Glucocorticoid genetics

KW - Transcription Factor AP-1 metabolism

KW - Animals

KW - Mice

KW - Mice, Knockout

KW - Apoptosis

KW - Cell Differentiation

KW - Osteogenesis drug effects

KW - Osteoblasts cytology

KW - Dimerization

KW - Glucocorticoids toxicity

KW - Interleukin-11 metabolism

KW - Receptors, Glucocorticoid genetics

KW - Transcription Factor AP-1 metabolism

M3 - SCORING: Zeitschriftenaufsatz

VL - 11

SP - 517

EP - 531

JO - CELL METAB

JF - CELL METAB

SN - 1550-4131

IS - 6

M1 - 6

ER -