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Review
. 2005 Jan 1:10:681-8.
doi: 10.2741/1563. Print 2005 Jan 1.

TGF-beta signaling in chondrocytes

Tian-Fang Li  1 , Regis J O'Keefe, Di Chen
Affiliations
Review

TGF-beta signaling in chondrocytes

Tian-Fang Li et al. Front Biosci. .

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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