Abstract
To elucidate the role of microRNA-219a (miR-219a) in the occurrence and progression of atherosclerosis. Transfection efficacy of miR-219a mimics and inhibitor was tested in vascular smooth muscle cells (VSMC). Proliferative and migratory capacities in ASMC regulated by miR-219a were examined by cell counting kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU) and Transwell assay, respectively. The target gene of miR-219a was predicted by bioinformatics method and confirmed by dual-luciferase reporter assay. Rescue experiments were conducted to clarify the role of miR-219a/HOXA1 axis in the progression of atherosclerosis. Overexpression of miR-219a attenuated proliferative and migratory capacities in ASMC. MiR-219a could bind HOXA1, and negatively regulate its mRNA and protein levels. Overexpression of HOXA1 promoted proliferative and migratory capacities in ASMC. Notably, co-overexpression of miR-219a and HOXA1 abolished the inhibitory effects of overexpressed miR-219a on proliferative and migratory capacities in ASMC. MiR-219a attenuates proliferative and migratory capacities in ASMC by binding HOXA1, thus participating in the progression of atherosclerosis.
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