Enhanced cellular fibronectin accumulation in chondrocytes treated with vitamin A.
Chick sternal chondrocytes cultured at high cell density lack fibronectin as a surface protein, while vitamin A-treated chondrocytes contain it as the major cell surface protein. We investigated the mechanism of fibronectin accumulation under these conditions. Control chondrocytes synthesized nearly as much fibronectin as vitamin A-treated chondrocytes, but it was secreted primarily into culture medium. Althought the fibronectin of control chondrocytes was of a slightly lower apparent molecular weight than the fibronectin synthesized by the treated cells, it bound as effectively to the cell layer of both normal and treated cells. In contrast, the vitamin A-treated cultures were 2.7 fold more effective in binding fibronectin synthesized by either control or treated cells. Thus in chondrocytes, vitamin A appears to regulate the cellular accumulation of fibronectin by increasing the ability of the cell layer to bind fibronectin rather than by altering its synthesis or its adhesivity for the cell layer.
D000818:Animals; D001665:Binding Sites; D002356:Cartilage / Q000187:drug effects* / Q000378:metabolism; D002454:Cell Differentiation; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D002645:Chickens; D005353:Fibronectins / Q000378:metabolism*; D008970:Molecular Weight; D014801:Vitamin A / Q000494:pharmacology*
D005353:Fibronectins; D014801:Vitamin A