Abstract
Cellular condensation of chondroprogenitors is a distinct cellular event in chondrogenesis. During this process, N-cadherin mediates cell-cell interactions responsible for the initial stage of cellular condensation and subsequently fibronectin contributes to cell-matrix interactions mediating a progression of chondrogenesis. We previously showed that chondrogenesis in mouse chondrogenic EC cells, ATDC5, was induced, at a high incidence in the presence of insulin, through formation of cellular condensation. In this study, we took advantage of the sequential progression of chondrogenesis in ATDC5 cells and evaluated, in vitro in these cells, the role of endogenous transforming growth factor (TGF)-β in chondrogenesis. ATDC5 cells expressed TGF-β 2 mRNA at a cellular condensation stage. The treatment of undifferentiated ATDCS cells with anti-TGF-β 2 neutralizing antibody inhibited the accumulatiOn of Alcian blue stainable proteoglycan in a dose-dependent manner. Transfection of a dominant-negative mutant of mouse TGF-β type II receptor to undifferentiated ATDC5 cells completely inhibited cellular condensation. Moreover, exogenously administered TGF-β 2 upregulated the expressron of fibronectin and type II collagen (a phenotypic marker gene of chondrogenesis) mRNAs and downregulated that of Ncadherin mRNA in time- and dose-dependent manners. These results indicate that TGF-β stimulates chondrogenesis via initiation of cellular condensation by transition from an initial N-cadherin-contributing stage to a fibronectin-contributing stage during processes of chondrogenesis in ATDCS cells.
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