The phenotype of vascular smooth muscle cells (SMCs) play important roles in atherogenesis. We studied roles of extracellular matrix (ECM) and platelet‐derived growth factor (PDGF)‐BB/interleukin (IL)‐1b in modulating SMC phenotype. Human aortic SMCs on monomeric collagen (MC) showed lower expression of contractile markers, with a higher percentage in the S‐phase, than the cells on polymerized collagen (PC). SMCs on PC had lower expressions of cyclin A, D1, and E, cyclin‐dependent protein kinase (Cdk) 2, 4, and 6, and higher expressions of p27 and p21, as compared with the cells on MC. PDGF‐BB/IL‐1b inhibited the contractile marker expression and induced cell cycle progression, with an increase in Cdk6 expression, in SMCs on PC. Transfection of SMCs with Cdk6‐siRNA inhibited the PDGF‐BB/IL‐1b‐induced cell cycle progression. Wortmannin and LY294002 inhibited the PDGF‐BB/IL‐1b‐induced Cdk6 expression in SMCs on PC. SMCs on MC showed higher levels of avb3 and lower levels of a2b1 integrins than the cells on PC. PDGF‐BB/IL‐1b inhibited the b1 and b3 expressions in SMCs on PC. Our findings provide insights into the molecular basis for the roles of ECM and PDGF‐BB/IL‐1b in modulating SMC phenotype.
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