MiR-30e-5p Alleviates Inflammation and Cardiac Dysfunction After Myocardial Infarction Through Targeting PTEN.

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Accumulating studies show that microRNAs are candidate biomarkers and therapeutic targets for cardiovascular diseases including myocardial infarction (MI). Bioinformatics analysis suggested that compared with Sprague-Dawley (SD) rats without MI, miR-30e-5p expression in the left ventricle tissue of SD rats with MI was significantly downregulated, suggesting miR-30e-5p may participate in the pathogenesis of MI. In this study, H9c2 cardiomyocytes were exposed to hypoxia to establish a hypoxic cell model. SD rats with left anterior descending coronary artery ligation were used for the MI animal model. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate the miR-30e-5p and PTEN mRNA expressions in cells and tissues. Western blot was used for detecting the expression of PTEN protein. miR-30e-5p expression in H9c2 cells was then inhibited or overexpressed, and its effects on viability and apoptosis were examined by cell counting kit-8 (CCK-8) assay and TUNEL assay, respectively. ELISA was used to detect inflammatory factors. The regulatory relationship between PTEN and miR-30e-5p was investigated by bioinformatics analysis, qRT-PCR, Western blot, and dual-luciferase reporter assay. It was found that miR-30e-5p expression was significantly downregulated in animal models and H9c2 cells under hypoxia. Overexpression of miR-30e-5p led to a dramatic increase of cell viability, accompanied by the decrease of IL-1β, TNF-α, IL-6, LDH, CK-MB, and cTnI. Furthermore, PTEN was identified as a target of miR-30e-5p, and PTEN overexpression reversed the effects of miR-30e -5p on H9c2 cells. To conclude, we confirm that miR-30e-5p alleviates inflammation and myocardial injury induced by MI via suppressing PTEN.