Journal
HUMAN CELL
Volume 34, Issue 2, Pages 349-359Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s13577-020-00466-z
Keywords
MicroRNA; Hypoxia; reoxygenation; Cardiomyocyte injury; Autophagy
Categories
Funding
- Shanghai Municipal Jiading District New Key Subject Program [2017-ZD-03]
- Shanghai Municipal Jiading District Health Commission Foundation [2019-KY-09]
- Natural Science Foundation of Shanghai [19ZR1444900]
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MicroRNAs (miRNAs) and autophagy play crucial roles in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury. The study identified miR-542-5p as a key regulator in H/R-induced cardiomyocyte injury, affecting cell viability, LDH activity, and apoptosis. The findings suggest that targeting the miR-542-5p/autophagy pathway could be a potential therapeutic strategy for H/R-related heart diseases.
MicroRNAs (miRNAs) and autophagy exert an important role in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury. The current study aimed to explore the role of miRNA and autophagy in H/R-induced cardiomyocyte injury. Cardiomyocyte H9c2 was exposed to H/R to simulate H/R injury in vitro. The differentially expressed miRNAs were identified using quantitative RT-PCR (qPCR). Lactate dehydrogenase (LDH) activity was assayed to assess H/R injury. The role of miRNA and autophagy in regulating the viability and cell apoptosis was evaluated using cell counting kit-8 (CCK-8) assay, flow cytometry (FCM), and western blot. The autophagy activation was assessed through testing the number of light chain 3 (LC3) puncta and LC3-II expression using western blot and immunofluorescence analysis. In the present study, we found that the miR-542-5p expression and the autophagy activation were significantly increased in H9c2 cells after H/R injury. Functionally, forced expression of miR-542-5p further aggravated H/R injury in H9c2 cells, whereas miR-542-5p inhibition alleviated H/R injury as measured by the cell viability, LDH activity and cell apoptosis. miR-542-5p repressed autophagy activation, whereas miR-542-5p inhibition facilitated autophagy activation in H9c2 cells exposed to H/R as measured by the LC3 puncta number, LC3II, and p62 protein level. Especially, autophagy inhibition by specific inhibitor partially lessened the role of miR-542-5p inhibitor in alleviating H/R injury. Finally, the autophagy-related 7 (ATG7) was identified as a novel target gene of miR-542-5p in H9c2 cells. The current data suggest that miR-542-5p/autophagy pathway might be a potential target for the treatment of H/R-related heart diseases.
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