Tributyltin and triphenyltin inhibit osteoclast differentiation through a retinoic acid receptor-dependent signaling pathway
- Research Institute for Biological Functions, Chubu University, 1200 Matsumoto, Kasugai-shi, Aichi 488-8501 (Japan)
- Department of Biological Chemistry, Chubu University, 1200 Matsumoto, Kasugai-shi, Aichi 487-8501 (Japan)
- Faculty of Biomedical Engineering, Toin University of Yokohama, 1614 Kurogane, Aoba, Yokohama, Kanagawa 225-8502 (Japan)
Organotin compounds, such as tributyltin (TBT) and triphenyltin (TPT), have been widely used in agriculture and industry. Although these compounds are known to have many toxic effects, including endocrine-disrupting effects, their effects on bone resorption are unknown. In this study, we investigated the effects of organotin compounds, such as monobutyltin (MBT), dibutyltin (DBT), TBT, and TPT, on osteoclast differentiation using mouse monocytic RAW264.7 cells. MBT and DBT had no effects, whereas TBT and TPT dose-dependently inhibited osteoclast differentiation at concentrations of 3-30 nM. Treatment with a retinoic acid receptor (RAR)-specific antagonist, Ro41-5253, restored the inhibition of osteoclastogenesis by TBT and TPT. TBT and TPT reduced receptor activator of nuclear factor-{kappa}B ligand (RANKL) induced nuclear factor of activated T cells (NFAT) c1 expression, and the reduction in NFATc1 expression was recovered by Ro41-5253. Our results suggest that TBT and TPT suppress osteoclastogenesis by inhibiting RANKL-induced NFATc1 expression via an RAR-dependent signaling pathway.
- OSTI ID:
- 20979851
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 355, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2006.12.237; PII: S0006-291X(06)02828-2; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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