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