MiR-93 inhibition ameliorates OGD/R induced cardiomyocyte apoptosis by targeting Nrf2.

Abstract:

OBJECTIVE:To identify the expression changes of microRNA 93 (miR-93) in oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes and its mechanism of mediating OGD/R and inducing apoptosis. MATERIALS AND METHODS:Primary cardiomyocytes were extracted and OGD/R model in cardiomyocytes was established in vitro. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expressions of miR-93, and Western blot assay was applied to measure the protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and caspase-3. Flow cytometry was utilized to examine the cardiomyocyte apoptosis rate. RESULTS:The apoptosis rate was increased after OGD/R in cardiomyocytes, accompanied by remarkable rise of miR-93 expression. After transfection of miR-93 antagomir, the apoptosis rate of cardiomyocyte induced by OGD/R was down-regulated, and the expression of cleaved caspase-3 was decreased. Meanwhile, the results of qRT-PCR and Western blot showed that the levels of Nrf2 mRNA and protein expression were up-regulated after the miR-93 level was inhibited, and luciferase reporter assay affirmed that Nrf2 was a target molecule for OGD/R-induced apoptosis mediated by miR-93. CONCLUSIONS:miR-93 mediates OGD/R-induced hypoxia/reoxygenation injury apoptosis in cells by targeting Nrf2.

authors

Yan LJ,Fan XW,Yang HT,Wu JT,Wang SL,Qiu CG

doi

10.26355/eurrev_201712_13935

subject

Has Abstract

pub_date

2017-12-01 00:00:00

pages

5456-5461

issue

23

eissn

1128-3602

issn

2284-0729

journal_volume

21

pub_type

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