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

被引：73

作者：

Li, Tian-Fang ^{[1
]}

Chen, Di ^{[1
]}

Wu, Qiuqian ^{[1
]}

Chen, Mo ^{[1
]}

Sheu, Tzong-Jen ^{[1
]}

Schwarz, Edward M. ^{[1
]}

Drissi, Hicham ^{[1
]}

Zuscik, Michael ^{[1
]}

O'Keefe, Regis J. ^{[1
]}

机构：

[1] Univ Rochester, Ctr Musculoskeletal Res, Dept Orthopaed, Rochester, NY 14642 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2006年 / 281卷 / 30期

关键词：

D O I：

10.1074/jbc.M600514200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

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.

引用

页码：21296 / 21304

页数：9

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