Abstract
MicroRNAs (miRNAs) are recognized to hold essential parts in the course of pathophysiology participating in myocardial ischemia/reperfusion (I/R) injury. The current study was intended to appraise the functional implication and underlying regulatory mechanism action of miR-20a in myocardial I/R injury. In cardiomyocyte hypoxia/reoxygenation (H/R) model simulating I/R, we observed that miR-20a was diminished in H9c2 cells subjected to H/R. The miR-20a mimics promoted cardiomyocyte viability and reduced H/R-triggered cell apoptosis, while the miR-20a inhibitors induced the inverse response in H9c2 cells subjected to H/R injury. Moreover, we ascertained that TLR4 was one downstream target gene of miR-20a and revealed that miR-20a might hold its protective action on cardiomyocytes subjected to H/R by inactivating p38 MAPK/JNK signaling. In summary, this study highlighted the relieved potential of miR-20a against cardiomyocyte H/R injury and suggested its favorable therapeutic role for myocardial I/R injury.
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XYG designed this study, directed all the experiments and wrote and revised the manuscript. YZ performed experiments, analyzed related data, and made figures. All authors have reviewed and agreed the manuscript.
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Editor: Tetsuji Okamoto
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Gong, XY., Zhang, Y. Protective effect of miR-20a against hypoxia/reoxygenation treatment on cardiomyocytes cell viability and cell apoptosis by targeting TLR4 and inhibiting p38 MAPK/JNK signaling. In Vitro Cell.Dev.Biol.-Animal 55, 793–800 (2019). https://doi.org/10.1007/s11626-019-00399-4
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DOI: https://doi.org/10.1007/s11626-019-00399-4