Title:MiR-30a-5p Promotes Vein Graft Restenosis by Inhibiting Cell
Autophagy through Targeting ATG5
Volume: 30
Issue: 6
Author(s): Xinyong Cai, Ping Zhang, Yong Yang, Yunxia Wang, Hongmin Zhu, Bin Li, Hong Zeng, Lang Hong and Liang Shao*
Affiliation:
- Department of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang
Medical College, Nanchang, Jiangxi 330000, P.R. China
Keywords:
Vein graft, restenosis, microRNA-30a-5p, ATG5, autophagy, intimal hyperplasia.
Abstract:
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.
