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Research Paper|Volume 15, Issue 21|pp 11875—11890

MicroRNA-30a-3p: a potential noncoding RNA target for the treatment of arteriosclerosis obliterans

Mao Zhang1, Yu Chen2, Fang Niu1, Xiaohui Luo3, Jiangping Li4, Wei Hu1
  • 1Department of Vascular Surgery, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, China
  • 2Department of Cardiology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, China
  • 3Department of Gynaecology and Obstetrics, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, China
  • 4Department of Oncological Radiotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China
* Equal contribution
Received: June 16, 2023Accepted: September 25, 2023Published: October 27, 2023
https://doi.org/10.18632/aging.205154

Copyright: © 2023 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

An increasing number of studies have shown that noncoding RNAs are involved in cardiovascular diseases. Our study shows that the expression of microRNA-30a-3p (miR-30a-3p) in patients with arteriosclerosis obliterans (ASO) of the lower extremities is significantly decreased after endovascular treatment, but its role is unclear. This study aims to explore the role of microRNA-30a-3p in ASO and its related mechanisms. Immunofluorescence and in situ hybridization costaining indicated that microRNA-30a-3p mostly exists in vascular smooth muscle cells (VSMCs). Furthermore, after transfection into VSMCs, microRNA-30a-3p inhibited VSMC proliferation, migration and phenotype switching. In addition, luciferase reporter and western blot analyses indicated that ROCK2 (Rho-related spiral coil 2 containing protein kinase) is a microRNA-30a-3p target gene, and participates in the microRNA-30a-3p mediated cell inhibitory effect. At last, the rat carotid artery was infected by lentivirus after balloon injury, which increased microRNA-30a-3p levels and apparently suppressed the formation of neointima in vivo. Overall, exogenous introduction of microRNA-30a-3p, a noncoding RNA with unlimited potential, may be a new approach to treat ASO.