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TGF-beta signaling in chondrocytes
Tian-Fang Li1,Regis J O'Keefe1,Di Chen1
1
Center for Musculoskeletal Research, Department of Orthopaedics, University of Rochester School of Medicine, Rochester, NY 14642, USA
DOI: 10.2741/1563 Volume 10 Issue 1, pp.681-688
Published: 01 January 2005
(This article belongs to the Special Issue TGFbeta,BMP receptor signaling)
Abstract

Transforming growth factor-beta (TGF-beta) regulates a large variety of cellular activities. Binding of TGF- beta to its cell surface receptor triggers several signaling cascades, among which the TGF- beta -Smad pathway is the most extensively studied. TGF- beta also activates protein kinases, including MAPK, PKA and PKC, and modulates gene expression via its delicate interaction with other signaling pathways. During endochondral bone formation, TGF- beta acts as a potent inhibitor of the terminal differentiation of epiphyseal growth plate chondrocytes. This effect appears to be primarily mediated by Smad molecules, although MAPK-ATF2 signaling is also involved. The rate of chondrocyte maturation is tightly regulated through the interactions of Smad-mediated signaling, the Wnt signaling pathway, and the transcription factor Runx2. Improving our understanding of the exact mechanisms underlying TGF- beta -mediated signaling pathways and their effects may greatly impact the diagnosis and treatment of many common orthopaedic diseases.

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Tian-Fang Li, Regis J O'Keefe, Di Chen. TGF-beta signaling in chondrocytes. Frontiers in Bioscience-Landmark. 2005. 10(1); 681-688.