Aim

At present, studies have focused on microRNAs (miRNAs) in myocardial ischemia-reperfusion injury (MI/RI). But the specific role of miR-30e hasn’t been fully explored. Thus, this study is to uncover the mechanism of miR-30e in MI/RI.

Methods

MI/RI models of rats and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established. Rats were injected with miR-30e and SRY-related high mobility group-box gene 9 (SOX9)-related oligonucleotides or vectors to explore their roles in MI/RI. H9C2 cardiomyocytes were transfected with restored miR-30e and depleted SOX9 to decipher their function in H/R injury. miR-30e and SOX9 expression in myocardial tissues and cardiomyocytes were detected. Online website prediction and luciferase activity assay were applied to validate the targeting relationship between miR-30e and SOX9.

Results

Decreased miR-30e and increased SOX9 were found in myocardial tissues of MI/RI rats and H/R-treated cardiomyocytes. miR-30e targeted SOX9. miR-30e up-regulation or SOX9 down-regulation reduced cardiac function damage and suppressed oxidative stress, inflammation, cardiomyocyte apoptosis and myocardial enzymes in myocardial tissues of MI/RI rats. Restoring miR-30e or silencing SOX9 energized cell viability and inhibited apoptosis of H/R-treated cardiomyocytes. Down-regulating SOX9 reversed the effects of miR-30e down-regulation on myocardial injury, ventricular remodeling, cardiomyocyte damage and apoptosis in MI/RI.

Conclusion

It is concluded that miR-30e elevation alleviated cardiac function damage and promoted ventricular remodeling via SOX9 repression.

中文翻译：

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microRNA-30e上调可减轻心肌缺血再灌注损伤，并通过SOX9抑制促进心室重构

目标

目前，研究集中在心肌缺血再灌注损伤（MI / RI）中的microRNA（miRNA）。但是，miR-30e的具体作用尚未得到充分研究。因此，本研究旨在揭示miR-30e在MI / RI中的机制。

方法

建立大鼠的MI / RI模型和H9C2心肌细胞的缺氧/复氧损伤（H / R）模型。向大鼠注射miR-30e和SRY相关的高迁移率族框基因9（SOX9）相关的寡核苷酸或载体，以探索它们在MI / RI中的作用。用还原的miR-30e转染H9C2心肌细胞并消耗SOX9以破译其在H / R损伤中的功能。检测到心肌组织和心肌细胞中的miR-30e和SOX9表达。应用在线网站预测和荧光素酶活性测定法验证了miR-30e和SOX9之间的靶向关系。

结果

在MI / RI大鼠和经H / R处理的心肌细胞的心肌组织中发现miR-30e降低和SOX9升高。miR-30e靶向SOX9。miR-30e上调或SOX9下调减少了MI / RI大鼠心肌组织的心脏功能损害，并抑制了氧化应激，炎症，心肌细胞凋亡和心肌酶。恢复miR-30e或沉默SOX9可增强细胞活力，并抑制经H / R处理的心肌细胞的凋亡。下调SOX9可以逆转miR-30e下调对MI / RI心肌损伤，心室重构，心肌细胞损伤和细胞凋亡的影响。

结论

结论是miR-30e升高通过SOX9抑制减轻了心功能损害并促进了心室重构。