期刊
BIOENGINEERED
卷 13, 期 1, 页码 280-290出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2021.2000229
关键词
Myocardial ischemia; reperfusion-induced injury; SOX2-OT; miR-186-5p; YY1
资金
- Inner Mongolia Natural Science Foundation project [2020MS08107, 2020MS08187, 2020MS08068]
- Inner Mongolia Medical University Youth Innovation Fund project [YKD2018QNCX052]
This study demonstrated for the first time that the long noncoding RNA SOX2-OT plays an important role in myocardial ischemia/reperfusion (MI/R) injury through regulating the miR-186-5p/YY1 axis. Inhibition of SOX2-OT attenuated cardiomyocyte dysregulation induced by oxygen-glucose deprivation/reoxygenation (OGD/R), with effects on relieving inflammation, promoting proliferation, and reducing apoptosis.
Long noncoding RNAs (lncRNAs) exert essential effects in regulating myocardial ischemia/reperfusion (MI/R)-induced injury. This work intended to explore the functions of lncRNA SOX2-OT and its regulatory mechanism within MI/R-induced injury. In this study, gene expression was determined by RT-qPCR. Western blotting was applied for the detection of protein levels. Pro-inflammatory cytokine concentrations, cardiomyocyte viability, and apoptosis were detected via ELISA, CCK-8 and flow cytometry. In the in vitro model, SOX2-OT and YY1 were both upregulated, while miR-186-5p was downregulated. SOX2-OT knockdown attenuated oxygen-glucose deprivation/reoxygenation (OGD/R)-induced cardiomyocyte dysregulation through relieving inflammation, promoting proliferation, and reducing apoptosis in OGD/R-treated H2C9 cells. SOX2-OT positively regulated YY1 expression via miR-186-5p. Moreover, miR-186-5p inhibition or YY1 upregulation abolished the effects of SOX2-OT blocking on the inflammatory responses, proliferation, and apoptosis of OGD/R-challenged H2C9 cells. In conclusion, our results, for the first time, demonstrated that SOX2-OT inhibition attenuated MI/R injury in vitro via regulating the miR-186-5p/YY1 axis, offering potential therapeutic targets for MI/R injury treatment.
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