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miR-1306-5p Alleviates Myocardial Cell Injury After Acute Myocardial Infarction Via Modulating TET3
Jinyuan Yi1, Fei Chai2, Sheng Li3
1Department of Cardiothoracic Vascular Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Abstract:
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.
Insights
MicroRNA-1306-5p is reduced in acute myocardial infarction (AMI) patients and predicts disease severity. Upregulating miR-1306-5p protects against cardiomyocyte damage by targeting NEAT1 and TET3.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- MicroRNAs (miRNAs) are crucial regulators in cardiovascular diseases like acute myocardial infarction (AMI).
- The specific role of miR-1306-5p in AMI pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the expression and function of miR-1306-5p in acute myocardial infarction.
- To explore the underlying molecular mechanisms of miR-1306-5p in regulating cardiomyocyte injury.
Main Methods:
- Real-time quantitative polymerase chain reaction (RT-qPCR) for gene expression analysis.
- Cell counting kit-8 (CCK-8) and Enzyme-Linked Immunosorbent Assay (ELISA) for cellular and inflammatory markers.
- Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.
Main Results:
- miR-1306-5p levels were significantly decreased in AMI patients and correlated with clinical indicators (cTnI, HDL-C, ejection fraction).
- Overexpression of miR-1306-5p reduced myocardial injury markers (cTnI, CK-MB) and inflammatory factors (TNF-α, IL-6, IL-1β) in hypoxia-reoxygenation treated cells.
- lncRNA NEAT1 acted as a molecular sponge for miR-1306-5p, and miR-1306-5p negatively regulated TET3 expression.
Conclusions:
- miR-1306-5p is a potential diagnostic and prognostic biomarker for AMI.
- miR-1306-5p protects cardiomyocytes from damage by interacting with NEAT1 and regulating TET3.
- Targeting the miR-1306-5p/NEAT1/TET3 axis may offer a therapeutic strategy for AMI.
