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Original Article

Korean J Physiol Pharmacol 2022; 26(3): 183-193

Published online May 1, 2022 https://doi.org/10.4196/kjpp.2022.26.3.183

Copyright © Korean J Physiol Pharmacol.

Differentially expressed mRNAs and their upstream miR-491-5p in patients with coronary atherosclerosis as well as the function of miR-491-5p in vascular smooth muscle cells

Hui Ding, Quanhua Pan, Long Qian, and Chuanxian Hu*

Department of Cardiovascular Surgery, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, Jiangsu 223300, China

Correspondence to:Chuanxian Hu
E-mail: huchuanxh@hotmail.com

Author contributions: H.D. and C.H. were the main designers of this study. H.D., Q.P., and L.Q. performed the experiments. C.H. analyzed the data. H.D. drafted the manuscript. All authors read and approved the final manuscript.

Received: September 10, 2021; Revised: November 1, 2021; Accepted: November 16, 2021

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

MicroRNAs (miRNAs) regulate gene expression and are biomarkers for coronary atherosclerosis (AS). A novel miRNA-mRNA regulation network of coronary AS still needs to be disclosed. The aim of this study was to analyze potential mRNAs in coronary AS patients and the role of their upstream miR-491-5p in vascular smooth muscle cells (VSMCs). We first confirmed top ten mRNAs according to the analysis from Gene Expression Omnibus database (GSE132651) and examined the expression levels of them in the plaques and serum from AS patients. Five mRNAs (UBE2G2, SLC16A3, POLR2C, PNO1, and AMDHD2) presented significantly abnormal expression in both plaques and serum from AS patients, compared with that in the control groups. Subsequently, they were predicted to be targeted by 11 miRNAs by bioinformatics analysis. Among all the potential upstream miRNAs, only miR-491-5p was abnormally expressed in the plaques and serum from AS patients. Notably, miR-491-5p overexpression inhibited viability and migration, and significantly increased the expression of contractile markers (α-SMA, calponin, SM22α, and smoothelin) in VSMCs. While silencing miR-491-5p promoted viability and migration, and significantly suppressed the expression of α-SMA, calponin, SM22α, and smoothelin. Overall, miR-491-5p targeted UBE2G2, SLC16A3, and PNO1 and regulated the dysfunctions in VSMCs.

Keywords: Coronary artery disease, miR-491-5p, PNO1, SLC16A3, UBE2G2

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