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J. Biol. Chem., Vol. 281, Issue 30, 21296-21304, July 28, 2006

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Transforming Growth Factor- Stimulates Cyclin D₁ Expression through Activation of -Catenin Signaling in Chondrocytes^*

From the Department of Orthopaedics, Center for Musculoskeletal Research, University of Rochester, Rochester, New York 14642

Transforming growth factor- (TGF-) plays an essential role in chondrocyte maturation. It stimulates chondrocyte proliferation but inhibits chondrocyte differentiation. In this study, we found that TGF- rapidly induced -catenin protein levels and signaling in murine neonatal sternal primary chondrocytes. TGF--increased -catenin induction was reproduced by overexpression of SMAD3 and was absent in Smad3^-/- chondrocytes treated with TGF-. SMAD3 inhibited -transducin repeat-containing protein-mediated degradation of -catenin and immunoprecipitated with -catenin following TGF- treatment. Both SMAD3 and -catenin co-localized to the nucleus after TGF- treatment. Although both TGF- and -catenin stimulated cyclin D₁ expression in chondrocytes, the effect of TGF- was inhibited with -catenin gene deletion or SMAD3 loss of function. These results demonstrate that TGF- stimulates cyclin D₁ expression at least in part through activation of -catenin signaling.

Received for publication, January 18, 2006 , and in revised form, March 17, 2006.

^* This work was supported by Grants AR38945 (to R. J. O.) and AR051189 (to D. C.) from the National Institutes of Health. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Both authors contributed equally to this work.

² To whom correspondence should be addressed: Dept. of Orthopaedics, University of Rochester Medical Center, P.O. Box 665, Rochester, NY 14642. Tel.: 585-273-5630; Fax: 585-275-1121; E-mail: regis_okeefe{at}urmc.rochester.edu.

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