MicroRNAs (miRNAs) has emerged as a key regulatory factor in cardiovascular diseases, including acute myocardial infarction (AMI). We aim to explore the effects of miR-1306-5p on AMI. We enrolled 130 AMI patients and 85 healthy individuals. The levels of genes were measured by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, myocardial injury markers and inflammatory factor levels were assessed via cell counting kit-8 (CCK-8) and Enzyme-Linked Immunosorbent Assay (ELISA) assays. Target relationships were confirmed via dual-luciferase reporter assays and RNA immunoprecipitation (RIP) experiments. miR-1306-5p was remarkably diminished in AMI patients. It was an independent predictor of AMI, showing a positive correlation with the cardiac troponin I (cTnI) and a negative correlation with high-density lipoprotein cholesterol (HDL-C) and ejection fraction. Mechanistically, upregulated miR-1306-5p diminished the levels of cTnI, creatine kinase-MB (CK-MB), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) while promoting proliferation in hypoxia-reoxygenation (H/R)-treated AC16 cells. These effects could be reversed by overexpressing ten-eleven translocation 3 (TET3). Moreover, lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was found to function as a microRNA sponge for miR-1306-5p. In conclusion, miR-1306-5p could bind to NEAT1 and subsequently mitigate cardiomyocyte damage by negatively regulating TET3.
Yi et al. (Wed,) studied this question.
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