TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) AND ARTICULAR CHONDROCYTES

Transforming growth factor-beta (TGF-beta) has a dual effect on the pr oliferation of joint chondrocytes. In medium with a low serum concentr ation, it inhibits cell growth, while in medium supplemented with 10% fetal calf serum it stimulates cell growth. This stimulation leads to a higher replication rate an a larger number of cells in the G2/M phas e of the cell cycle. Since these cells have already replicated their D NA, they can begin mitosis when stimulated by a EGF type factor. This mechanism involves the systems of the TGF-beta receptors which appear to vary with the cell cycle. In addition, a glycane inositophosphate m ay play a role as a second messenger for TGG-beta in this action. Fina lly, TGF-beta cannot restore the chondrocyte phenotype in dedifferenti ated cells nor limit the dedifferentiation process. It exerts a opposi ng effect to the deleterious effects of interleukin-I by inhibiting th e expression of the receptors of this cytokine at the level of transcr iption. These in vitro effects would suggest that TGF-beta plays an im portant role in the repair potentiality of joint cartilage especially in arthrosis. In vivo studies are however necessary to verify this hyp othesis.