miR-1306-5p Alleviates Myocardial Cell Injury After Acute Myocardial Infarction Via Modulating TET3

MicroRNAs (miRNAs) has emerged as a key regulatory factor in cardiovascular diseases, including acute myocardial infarction (AMI). We aim to explore the effects of <i>miR-1306-5p</i> 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. <i>miR-1306-5p</i> 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 <i>miR-1306-5p</i> 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 <i>ten-eleven translocation 3 (TET3)</i>. Moreover, lncRNA <i>nuclear paraspeckle assembly transcript 1 (NEAT1)</i> was found to function as a microRNA sponge for <i>miR-1306-5p</i>. In conclusion, <i>miR-1306-5p</i> could bind to <i>NEAT1</i> and subsequently mitigate cardiomyocyte damage by negatively regulating <i>TET3</i>.