LAUSR

OBJECTIVE To investigate the role of miR-30a-5p in restenosis of rats following vein grafting and the underlying mechanism. METHODS Vein graft rat models were established and perfused with miR-30a-5p antagomir and si-ATG5 to probe the regulation of miR-30a-5p/ATG5 on intimal hyperplasia. Human saphenous vein smooth muscle cells (HSVSMCs) were obtained from the great saphenous veins of patients undergoing coronary artery bypass grafting and subjected to assays for autophagy, proliferation and migration after gain and loss of function of miR-30a-5p and/or ATG5. The binding of miR-30a-5p and ATG5 was confirmed by RIP and dual-luciferase reporter assays. RESULTS MiR-30a-5p expression gradually increased, ATG5 expression gradually decreased, and the intima were increasingly thickened during restenosis of grafted veins. Knockdown of miR-30a-5p in rats repressed the restenosis of vein grafts, while a deficiency of ATG5 reversed the effect of miR-30a-5p inhibition. Upregulation of miR-30a-5p enhanced the proliferation and migration of HSVSMCs and inhibited autophagy, while downregulation of miR-30a-5p or overexpression of ATG5 showed opposite effects. ATG5 was a target gene of miR-30a-5p. CONCLUSION MiR-30a-5p exacerbates vein graft restenosis by repressing ATG5 expression and inhibiting autophagy.