ORIGINAL ARTICLE   

Panminerva Medica 2022 March;64(1):31-7

DOI: 10.23736/S0031-0808.20.03929-4

Copyright © 2020 EDIZIONI MINERVA MEDICA

language: English

MiR-379 relieves myocardial injury after acute myocardial infarction by regulating tumor necrosis factor-α-induced protein 8

Haiyue DAI ✉, Xiaojun JI, Xumei HUANG, Weixin LI, Zhongping SHI

Department of Cardiology, Wenzhou Central Hospital, Wenzhou, China

BACKGROUND: Acute myocardial infarction (AMI) is the myocardial avascular necrosis syndrome caused by coronary atherosclerotic plaque rupture, thrombosis or coronary artery occlusion. Therefore, it is of great significance to find new targets for the treatment of myocardial infarction. The purpose of this study was to investigate the effect of microRNA-379 (miR-379) on AMI and its mechanism.
METHODS: MiR-379 mimic was used to transfect H9c2 cells and we determined the protective effect of miR-379 on H9c2 by detecting the level of apoptosis. TargetScan software was used to detect miR-379’s downstream targets. We constructed siRNA to analyze the effect of miR-379’s downstream targets on H9c2 cells. In addition, we used miR-379 agomir to inject the tail vein of AMI rats to verify the effect of miR-379 on rat cardiomyocytes.
RESULTS: TargetScan detected that miR-379 and Tumor necrosis factor-α-induced protein 8 (TNFAIP8) may have binding sites and the dual luciferase reporter assay found that miR-379 binds to TNFAIP8 and inhibits its activity. MiR-379 mimic was found to reduce the expression of caspase3 and caspase9 in H9c2 cells and thereby reduce H2O2-induced cell damage. Inhibition of TNFAIP8 also significantly reduced apoptosis level and inhibited the NF-κB signaling pathway in H9c2 cells. Finally, miR-379 agomir was used to inject the tail vein of AMI rats and verified the protective effect of miR-379 in the heart in vivo.
CONCLUSIONS: MiR-379 has a binding site with TNFAIP8 and can inhibit its activity by binding to TNFAIP8 mRNA. SiRNA-TNFAIP8 can inhibit the NF-κB signaling pathway and protect myocardial cells from AMI-induced myocardial damage by reducing the apoptosis level of myocardial cells.

KEY WORDS: Human MIRN379 microRNA; Myocardial infarction; tumor necrosis factor-alpha; Human TNFAIP8L1 protein