miR-133b inhibits myocardial ischemia-reperfusion-induced cardiomyocyte apoptosis and accumulation of reactive oxygen species in rats by targeting YES1.
10.12122/j.issn.1673-4254.2020.10.03
- Author:
Xing PENG
1
;
Ling LIN
1
;
Xiangqun ZHOU
1
;
Daying YANG
1
;
Yang CAO
2
;
Taoyuan YIN
1
;
Yuanyuan LIU
3
Author Information
1. Department of Cardiovascular Medicine, Sanya Central Hospital, Sanya 572000, China.
2. Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin 150000, China.
3. Department of Cardiology, Heilongjiang Provincial Hospital, Harbin 150000, China.
- Publication Type:Journal Article
- Keywords:
YES1;
apoptosis;
miR-133b;
myocardial ischemia-reperfusion;
reactive oxygen species
- MeSH:
Animals;
Apoptosis;
MicroRNAs/genetics*;
Myocardial Reperfusion Injury;
Myocytes, Cardiac;
Rats;
Rats, Sprague-Dawley;
Reactive Oxygen Species
- From:
Journal of Southern Medical University
2020;40(10):1390-1398
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of miR-133b on cardiomyocyte apoptosis induced by myocardial ischemia-reperfusion (I/R) and explore the mechanism.
METHODS:Thirty-six adult SD rats were randomized into sham-operated group, I/R group, AdmiR-NC group and AdmiR-133b group, and rat models of myocardial I/R were established in the latter 3 groups with myocardial injections of saline or recombinant adenoviruses in the left ventricle. The expression of MiR-133b was detected using RT-qPCR, and cardiac function of the rats was determined using FDP 1 HRV and BRS analysis system. Serum CK-MB and cTnI levels were determined by ELISA, myocardial injury was evaluated with HE staining, cardiomocyte apoptosis was detected by flow cytometry, and ROS content was determined using a DCFH-DA probe. In the in vitro experiment, H9C2 myocardial cells with hypoxia/reoxygenation (H/R) treatment were transfected with Mir-NC or MiR-133b mimic, and the cellular expression of MiR-133b, cell apoptosis, and ROS content were determined. Dual luciferase reporter assay was performed to verify the targeting relationship between miR-133b and YES1. The effects of pc-YES1 or miR-133b mimic transfection on YES1 expression, apoptosis, and ROS content in H9C2 cells were evaluated.
RESULTS:Compared with those in I/R group, miR-133b expression was obviously up-regulated, LVEDP, cTnI and CK-MB levels were significantly decreased, and LVSP, +dp/dt, -dp/dt, HR and CF levels were increased in admiR-133b group (
CONCLUSIONS:miR-133b can inhibit I/R-induced myocardial cell apoptosis and ROS accumulation by targeting YES1 to reduce myocardial I/R injury in rats.
