MiR-32-3p Regulates Myocardial Injury Induced by Microembolism and Microvascular Obstruction by Targeting RNF13 to Regulate the Stability of Atherosclerotic Plaques

• Published in: Journal of cardiovascular translational research Vol. 15; no. 1; pp. 143 - 166
• Main Authors: Huang, Dajun, Liu, Yang, Gao, Le, Wei, Xiaomin, Xu, Yuli, Cai, Ruping, Su, Qiang
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.02.2022
• Subjects: Animals; Antagomirs - metabolism; Apoptosis; Apoptosis Regulatory Proteins - metabolism; Biomedical Engineering and Bioengineering; Biomedicine; Cardiology; Endoplasmic Reticulum Stress; Human Genetics; Human Umbilical Vein Endothelial Cells - metabolism; Humans; Medicine; Medicine & Public Health; MicroRNAs - genetics; MicroRNAs - metabolism; Myocardial Infarction - genetics; Myocardial Infarction - pathology; Original Article; Plaque, Atherosclerotic - genetics; Plaque, Atherosclerotic - pathology; Rats; Ubiquitin-Protein Ligases - genetics; Ubiquitin-Protein Ligases - metabolism; Myocardium; Atherosclerotic plaque stability; MiR-32-3p; RNF13; Embolism
• ISSN: 1937-5387; 1937-5395
• DOI: 10.1007/s12265-021-10150-8

This study aimed to explore the molecular mechanism of myocardial protection. The effects of miR-32-3p and ring finger protein 13 (RNF13) on endoplasmic reticulum (ER) stress-induced apoptosis of A-10 cells and human umbilical vein endothelial cells (HUVEC) were detected using flow cytometry. The effects of miR-32-3p and phenylbutyric acid (PBA) on plaque instability and myocardial tissue injury in rats were investigated after establishment of arterial plaque model and embolization model and treatment with miR-32-3p-antagomir and PBA. RNF13, which was differentially expressed in myocardial infarction, was the direct target gene of miR-32-3p. MiR-32-3p inhibited RNF13 expression and targeted RNF13 to inhibit ER stress-induced cell apoptosis. Furthermore, inhibiting miR-32-3p expression induced arterial plaque instability by reducing survival, increasing pathological lesions in arterial tissue, up-regulating ER stress-related proteins, and regulating the expressions of apoptosis-related proteins in the model rats. However, PBA reversed the effects of miR-32-3p-antagomir on the model rats. Graphical abstract MiR-32-3p regulates myocardial injury induced by micro-embolism and micro-vascular obstruction by targeting RNF13 to regulate the stability of atherosclerotic plaques