MiR-195 enhances cardiomyocyte apoptosis induced by hypoxia/reoxygenation injury via downregulating c-myb.

Abstract:

OBJECTIVE:In this study, we explored the regulative effect of miR-195 on c-myb expression and also investigated the role of miR-195 and c-myb in cardiomyocyte apoptosis induced by hypoxia/reoxygenation (H/R) injury. MATERIALS AND METHODS:QRT-PCR analysis was performed to measure mature miR-195 expression. H9c2 cells were transfected for miR-195 overexpression or knockdown or c-myb overexpression using Lipofectamine 2000. The cells were subjected to H/R treatment and following flow cytometric analysis of active caspase-3 or florescent study of reactive oxygen species (ROS) generation. The binding sites between miR-195 and 3'UTR of MYB mRNA were predicted using TargetScan 7.0. The binding sites were verified using dual luciferase assay and Western blot analysis. RESULTS:MiR-195 is significantly upregulated after H/R treatment in H9c2 cells. H/R injury induced active caspase-3 expression. However, the cells with miR-195 suppression had substantially lower ratio of cells with active caspase-3. MiR-195 can decrease c-myb protein expression. Dual luciferase assay verified two binding sites between miR-195 and 3'UTR of MYB mRNA. C-myb overexpression can suppress mitochondrial superoxide generation and cardiomyocyte apoptosis after H/R. CONCLUSIONS:MiR-195 is significantly increased due to H/R and can enhance cardiomyocyte apoptosis. MYB is a target gene of miR-195 in cardiomyocytes. The miR-195-MYB axis is involved in regulation of cardiomyocyte apoptosis induced by H/R.

authors

Chen C,Jia KY,Zhang HL,Fu J

subject

Has Abstract

pub_date

2016-08-01 00:00:00

pages

3410-6

issue

16

eissn

1128-3602

issn

2284-0729

journal_volume

20

pub_type

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