Transforming growth factor-beta stimulates cyclin D1 expression through activation of beta-catenin signaling in chondrocytes |
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Authors: | Li Tian-Fang Chen Di Wu Qiuqian Chen Mo Sheu Tzong-Jen Schwarz Edward M Drissi Hicham Zuscik Michael O'Keefe Regis J |
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Institution: | Department of Orthopaedics, Center for Musculoskeletal Research, University of Rochester, New York 14642, USA. |
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Abstract: | Transforming growth factor-beta (TGF-beta) plays an essential role in chondrocyte maturation. It stimulates chondrocyte proliferation but inhibits chondrocyte differentiation. In this study, we found that TGF-beta rapidly induced beta-catenin protein levels and signaling in murine neonatal sternal primary chondrocytes. TGF-beta-increased beta-catenin induction was reproduced by overexpression of SMAD3 and was absent in Smad3(-/-) chondrocytes treated with TGF-beta. SMAD3 inhibited beta-transducin repeat-containing protein-mediated degradation of beta-catenin and immunoprecipitated with beta-catenin following TGF-beta treatment. Both SMAD3 and beta-catenin co-localized to the nucleus after TGF-beta treatment. Although both TGF-beta and beta-catenin stimulated cyclin D(1) expression in chondrocytes, the effect of TGF-beta was inhibited with beta-catenin gene deletion or SMAD3 loss of function. These results demonstrate that TGF-beta stimulates cyclin D(1) expression at least in part through activation of beta-catenin signaling. |
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