miR‐200a‐3p inhibits the PDGF‐BB‐induced proliferation of VSMCs by affecting their phenotype‐associated proteins

Abstract

AbstractAccumulating evidence shows that the abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) can significantly affect the long‐term prognosis of coronary artery bypass grafting. This study aimed to explore the factors affecting the proliferation, migration, and phenotypic transformation of VSMCs. First, we stimulated VSMCs with different platelet‐derived growth factor‐BB (PDGF‐BB) concentrations, analyzed the expression of phenotype‐associated proteins by Western blotting, and examined cell proliferation by scratch wound healing and the 5‐ethynyl‐2‐deoxyuridine (EdU) assay. VSMC proliferation was induced most by PDGF‐BB treatment at 20 ng/mL. miR‐200a‐3p decreased significantly in A7r5 cells stimulated with PDGF‐BB. The overexpression of miR‐200a‐3p reversed the downregulation of α‐SMA (p < 0.001) and the upregulation of vimentin (p < 0.001) caused by PDGF‐BB. CCK8 and EdU analyses showed that miR‐200a‐3p overexpression could inhibit PDGF‐BB‐induced cell proliferation (p < 0.001). However, flow cytometric analysis showed that it did not significantly increase cell apoptosis. Collectively, the overexpression of miR‐200a‐3p inhibited the proliferation and migration of VSMCs induced by PDGF‐BB, partly by affecting phenotypic transformation‐related proteins, providing a new strategy for relieving the restenosis of vein grafts.