Vascular smooth muscle cells (V-SMC) alter their functions from contraction to production of extracellular matrices during the response to injury of the arterial wall. Accumulation of these matrices characterize the chronic structural change of arteriosclerosis. In this paper, we reported as follows.(1) V-SMC freshly isolated from human aortic media had strong reactivity with anti-smooth muscle specific alpha-actin (alpha-SM actin) antibody but not with anti-prolyl 4-hydroxylase (ProHy) antibody.(2) The exponentially growing cells in serum-containing culture media reduced alpha-SM actin and induced ProHy distinctly.(3) Growth-arrested cells with serum starvation rearranged numerous alpha-SM actin fibers in their cytoplasm. And the rearrangement of contractile filaments inhibited by the addition of single competence growth factor, such as platelet derived growth factor (PDGF) or basic fibroblast growth factor (bFGF). These results suggest that V-SMC change their phenotype in a competence-factor-dependent manner.