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Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor
Vise andre og tillknytning
2010 (engelsk)Inngår i: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 11, nr 6, s. 517-531Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
2010. Vol. 11, nr 6, s. 517-531
Emneord [en]
induced osteoporosis; gene-expression; dna-binding; cell-cycle; mice; inhibition; interleukin-11; osteoclast; mechanisms; phenotype
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Forskningsprogram
odontologi
Identifikatorer
URN: urn:nbn:se:umu:diva-40517DOI: 10.1016/j.cmet.2010.05.005ISI: 000278747800010PubMedID: 20519123OAI: oai:DiVA.org:umu-40517DiVA, id: diva2:400270
Tilgjengelig fra: 2011-02-25 Laget: 2011-02-25 Sist oppdatert: 2018-06-08bibliografisk kontrollert

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