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Literature DB >> 16690606

Transforming growth factor-beta stimulates cyclin D1 expression through activation of beta-catenin signaling in chondrocytes.

Tian-Fang Li¹, Di Chen, Qiuqian Wu, Mo Chen, Tzong-Jen Sheu, Edward M Schwarz, Hicham Drissi, Michael Zuscik, Regis J O'Keefe.

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.

Entities: Gene Species

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Year: 2006 PMID： 16690606 PMCID： PMC2649822 DOI： 10.1074/jbc.M600514200

Source DB: PubMed Journal: J Biol Chem ISSN： 0021-9258 Impact factor: 5.157

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