Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 10, Issue -, Pages 681-688Publisher
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/1563
Keywords
TGF-beta; receptor; Smad; chondrocyte; maturation; review; gene
Categories
Funding
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR038945, R03AR048920, R01AR051189] Funding Source: NIH RePORTER
- NIAMS NIH HHS [R01 AR051189-01, R01-AR051189, R01 AR038945, R01-AR38945, R01 AR051189, R03 AR048920-01A1, R03 AR048920-02, R03 AR048920, R03-AR48920] Funding Source: Medline
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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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