MiR-30a-5p Promotes Vein Graft Restenosis by Inhibiting Cell Autophagy through Targeting ATG5

Objective The aim of the study was 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 was 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 the autophagy, while downregulation of miR-30a-5p or overexpression of ATG5 showed opposite effects. ATG5 is a target gene of miR-30a-5p. Conclusion MiR-30a-5p exacerbates vein graft restenosis by repressing ATG5 expression and inhibiting autophagy.

Automated summary

The study aimed to investigate the role of miR-30a-5p in restenosis following vein grafting in rats and its underlying mechanism. The results showed that miR-30a-5p expression gradually increased, ATG5 expression gradually decreased, and the intima thickened during restenosis. It was concluded that miR-30a-5p exacerbates vein graft restenosis by repressing ATG5 expression and inhibiting autophagy.