Autoimmunity (May 2021)

Modulation of miR-382-5p reduces apoptosis of myocardial cells after acute myocardial infarction

  • Liqin Zhang,
  • Huajie Zhu,
  • Xianlin Teng,
  • Xiaosheng Sheng,
  • Beiwei Yu

DOI
https://doi.org/10.1080/08916934.2021.1910812
Journal volume & issue
Vol. 54, no. 4
pp. 195 – 203

Abstract

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Background Acute myocardial infarction (AMI) is a severe cardiovascular condition. Blocking the apoptosis of myocardial cells may mitigate AMI. Excessive expression of Stanniocalcin-1 (STC1) plays a protective role in the heart by inhibiting myocardial cell apoptosis. Here, we looked at the mechanism by which miR-382-5p regulates STC1 and affects myocardial cell apoptosis after AMI. Methods An AMI mouse model with a descending anterior ligament coronary artery and an HL-1 cell model with reproducible hypoxia/reoxygenation (H/R) were established. For pathological changes in myocardial tissues, terminal deoxynucleotidyl transferase dUTP nick end labelling staining and haematoxylin and eosin staining were performed. STC1 mRNA and miR-382-5p levels were measured using quantitative real-time PCR. Protein levels of STC1 and apoptosis-related proteins were measured by western blotting. The 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide assay was used to detect cell viability, and a dual-luciferase reporter assay was carried out to verify potential targets of miR-382-5p. Results The level of miR-382-5p was raised in myocardial tissues of AMI mice and H/R-induced HL-1 cells. Compared with the control group, the myocardial tissue cells in the AMI group were disordered, with evident necrosis of myocardial cells, apoptosis and inflammatory infiltration. Interference with miR-382-5p inhibited myocardial cell apoptosis after H/R, as well as inferior lactate dehydrogenase. Also, miR-382-5p adversely regulated STC1 and the expression of STC1 was increased after transfection with miR-382-5p antagomir. Furthermore, interference with miR-382-5p reduced myocardial cell apoptosis after H/R by increasing the expression level of STC1. Conclusion To summarise, our study showed an increase in miR-382-5p in myocardial tissues in the AMI mouse model. Interference with miR-382-5p reduced apoptosis of myocardial cells after AMI and the effect was achieved by increasing STC1 expression.

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