miR-27a-5p Attenuates Hypoxia-induced Rat Cardiomyocyte Injury by Inhibiting Atg7.
Jinwei ZhangWanling QiuJideng MaYujie WangZihui HuKeren LongXun WangLong JinQianzi TangGuoqing TangLi ZhuXuewei LiSurong ShuaiMingzhou LiPublished in: International journal of molecular sciences (2019)
Acute myocardial infarction (AMI) is an ischemic heart disease with high mortality worldwide. AMI triggers a hypoxic microenvironment and induces extensive myocardial injury, including autophagy and apoptosis. MiRNAs, which are a class of posttranscriptional regulators, have been shown to be involved in the development of ischemic heart diseases. We have previously reported that hypoxia significantly alters the miRNA transcriptome in rat cardiomyoblast cells (H9c2), including miR-27a-5p. In the present study, we further investigated the potential function of miR-27a-5p in the cardiomyocyte response to hypoxia, and showed that miR-27a-5p expression was downregulated in the H9c2 cells at different hypoxia-exposed timepoints and the myocardium of a rat AMI model. Follow-up experiments revealed that miR-27a-5p attenuated hypoxia-induced cardiomyocyte injury by regulating autophagy and apoptosis via Atg7, which partly elucidated the anti-hypoxic injury effects of miR-27a-5p. Taken together, this study shows that miR-27a-5p has a cardioprotective effect on hypoxia-induced H9c2 cell injury, suggesting it may be a novel target for the treatment of hypoxia-related heart diseases.
Keyphrases
- acute myocardial infarction
- cell cycle arrest
- oxidative stress
- induced apoptosis
- endoplasmic reticulum stress
- cell death
- signaling pathway
- endothelial cells
- single cell
- pi k akt
- heart failure
- angiotensin ii
- stem cells
- poor prognosis
- percutaneous coronary intervention
- atrial fibrillation
- ischemia reperfusion injury
- type diabetes
- rna seq
- dna methylation
- transcription factor
- blood brain barrier
- long non coding rna
- bone marrow
- genome wide