miR-133b inhibits myocardial ischemia-reperfusion-induced cardiomyocyte apoptosis and accumulation of reactive oxygen species in rats by targeting YES1

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 (P < 0.01). The rats in admiR-133b group showed obviously reduced pathological damage, cell apoptosis and ROS content compared with those in I/ R group (P < 0.01). In H9C2 cells exposed to H/R, transfection with miR-133b mimic significantly up-regulated miR-133b expression and decreased cell apoptosis and ROS content (P < 0.01). The results of dual luciferase reporter assay suggested a direct targeting relationship between miR-133b and YES1, and MiR-133b mimic transfection significantly down-regulated YES1 protein expression in cells with H/R exposure (P < 0.01). Co-transfection with pc-YES1 reversed the effect of miR-133b overexpression on myocardial cell apoptosis and ROS accumulation.

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.

Medienart:

E-Artikel

Erscheinungsjahr:

2020

Erschienen:

2020

Enthalten in:

Zur Gesamtaufnahme - volume:40

Enthalten in:

Nan fang yi ke da xue xue bao = Journal of Southern Medical University - 40(2020), 10 vom: 30. Okt., Seite 1390-1398

Sprache:

Chinesisch

Beteiligte Personen:

Peng, Xing [VerfasserIn]
Lin, Ling [VerfasserIn]
Zhou, Xiangqun [VerfasserIn]
Yang, Daying [VerfasserIn]
Cao, Yang [VerfasserIn]
Yin, Taoyuan [VerfasserIn]
Liu, Yuanyuan [VerfasserIn]

Links:

Volltext

Themen:

Apoptosis
Journal Article
MiR-133b
MicroRNAs
Myocardial ischemia-reperfusion
Reactive Oxygen Species
Reactive oxygen species
YES1

Anmerkungen:

Date Completed 02.11.2020

Date Revised 02.09.2022

published: Print

Citation Status MEDLINE

doi:

10.12122/j.issn.1673-4254.2020.10.03

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM316870978