The phenotypic transition of smooth muscle cells (SMC) from a contractile to a synthetic state appears to be an early event in the pathogenesis of atherosclerosis. It was found that plasma fibronectin promotes the transition of rat aortic SMC into the synthetic phenotype and that laminin delays this process. Recently, we found that type I collagen is as efficient as fibronectin in promoting the initial attachment and phenotypic transition of rabbit arterial SMC and elastin maintained the cells in the contractile phenotype, as laminin. On the other hand, laminin plus type IV collagen suggest that a partial remodulation may be possible. These findings emphasize the importance of extracellular matrix components in the control of the differentiated properties of arterial SMC and may be important for clarifying the development of atherosclerosis.