Retinoic acid (RA) treatment of a suspension of quail chondrocytes inhibits the expression of cartilage collagens and induces cell adhesion along with fibronectin expression. We asked whether the RA-induced modulation of the chondrocyte phenotype was dependent on cell adhesion. Prevention of cell adhesion blocks cell growth and many of the effects associated with RA, such as collagen II inhibition, collagen I activation and fibronectin induction. The activity of the bone/tendon promoter of the α2(I) collagen gene was determined by measuring the transient expression of COL1A2-CAT, a chimaeric gene bearing 3500 bp from upstream of the transcription start site of the human α2(I) gene fused to the chloramphenicol acetyltransferase (CAT) gene. This promoter is activated only in permissive conditions for cell adhesion. The attachment activities of chondrocytes on protein substrates was studied by an in vitro cell adhesion assay. Untreated cells or cells maintained in suspension while undergoing RA treatment do not attach when replated on protein substrates. Chondrocytes treated with RA in permissive conditions for cell adhesion rapidly attach and spread instead on collagen-coated wells. Altogether the results suggest that cell adhesion plays a major role in RA-induced modulation of the chondrocyte phenotype.
|Number of pages||6|
|Publication status||Published - Jan 1 1996|
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