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dc.contributor.authorMartina Rauneren_US
dc.contributor.authorSylvia Thieleen_US
dc.contributor.authorKathrin Sinningenen_US
dc.contributor.authorMaria Winzeren_US
dc.contributor.authorJuliane Salbach-Hirschen_US
dc.contributor.authorIna Gloeen_US
dc.contributor.authorKatrin Peschkeen_US
dc.contributor.authorGuy Haegemanen_US
dc.contributor.authorJan P. Tuckermannen_US
dc.contributor.authorLorenz C. Hofbaueren_US
dc.contributor.otherDresden University Faculty of Medicine and University Hospital Carl Gustav Carusen_US
dc.contributor.otherTechnische Universitat Dresdenen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherUniversitat Ulmen_US
dc.identifier.citationEndocrinology. Vol.154, No.10 (2013), 3719-3728en_US
dc.description.abstractGlucocorticoids (GCs) are potent drugs to treat rheumatoid arthritis but exert adverse skeletal effects. Compound A (CpdA) is a selective GC receptor modulator with an improved risk/benefit profile in mouse models of inflammation and bone loss. Here we tested whether CpdA also exerts bone-sparing effects under proinflammatory circumstances using the collagen-induced arthritis model, a murine model of rheumatoid arthritis. CpdA decreased disease activity, paw swelling, and the paw temperature by 43%, 12%, and 7%, respectively, but was less potent than dexamethasone (DEX), which reduced these parameters by 72%, 22%, and 10%, respectively. Moreover, T cells isolated from CpdA- and DEX-treated animals were less active based on proliferation rates after challenge with type II collagen and produced smaller amounts of interferon-γ and TNF as compared with T cells from PBS-treated mice. Histological assessment of the joints confirmed the weaker potency of CpdA as compared with DEX in preventing infiltration of inflammatory cells, induction of osteoclastogenesis, and destruction of articular cartilage. Due to the lack of GC-susceptible arthritis models, we were not able to fully address the bone-sparing potential of CpdA in inflammatory conditions. Nevertheless, the bone formation marker procollagen type 1 N-terminal peptide, a surrogate marker for GC-mediated suppression of bone formation, was significantly decreased by DEX in arthritic mice but not by CpdA. Our data indicate that CpdA moderately suppresses inflammation, whereas the concurrent effects on bone remain unknown. In light of its narrow therapeutic range, CpdA may be more useful as a molecular tool for dissecting GC actions rather than a therapeutic agent. Copyright © 2013 by The Endocrine Society.en_US
dc.rightsMahidol Universityen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleEffects of the selective glucocorticoid receptor modulator compound a on bone metabolism and inflammation in male mice with collagen-induced arthritisen_US
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