Abstract
PurposeAtherosclerosis (AS) is a chronic cardiovascular disease that seriously endangers human health. Our previous studies have shown that the expression of miR-205–5p is significantly reduced in the AS model of ApoE-/- mice, which has attracted our attention. This study aimed to explore the role and molecular mechanism of miR-205–5p in the progression of human aortic vascular smooth muscle cells (HAVSMCs) MethodsUse ox-LDL to induce HAVSMCs to construct an in vitro cell model of AS, and silence/overexpress miR-205–5p. Use MTT, cell flow cytometry, wound healing experiments, RT-qPCR and Western blot to explore the role and mechanism of miR-205–5p. ResultsmiR-205–5p can reduce the cell viability of HAVSMCs induced by ox-LDL; inhibit the expression of cyclin D1 to inhibit the cell cycle; increase the expression of Bax/Bcl-2 and Cleaved-caspase3 to promote cell apoptosis; inhibit proliferation and migration. RT-qPCR and Western blot results showed that miR-205–5p can inhibit the phosphorylation of ERBB4 and AKT in HAVSMCs induced by ox-LDL ConclusionmiR-205–5p can inhibit the proliferation and migration of HAVSMCs induced by ox-LDL, revealing its possibility of becoming a new target for alleviating AS.
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