MicroRNA‑138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria‑mediated apoptosis by targeting HIF1‑α

• Published in: Experimental and therapeutic medicine Vol. 18; no. 5; pp. 3325 - 3332
• Main Authors: Liu, Yan, Zou, Jianfeng, Liu, Xiaoyan, Zhang, Quan
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications UK Ltd 01-11-2019; D.A. Spandidos
• Subjects: Apoptosis; Cardiomyocytes; Cardiovascular disease; Diabetes; Gene expression; Hypoxia; Ischemia; Laboratory animals; Membranes; MicroRNAs; Mitochondria; Phosphorylation; Proteins; United States > US; China
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2019.7976

Myocardial ischemia-reperfusion (I/R) injury is considered to have a detrimental role in coronary heart disease, which is considered to be the leading cause of death worldwide. However, the molecular mechanism involved in the progression of myocardial I/R injury is still unclear. The current study aimed to investigate the expression and function of microRNA (miR)-138 in the process of myocardial I/R injury. First, miR-138 expression levels were analyzed both in myocardium with I/R injury and control myocardium using reverse transcription-quantitative polymerase chain reaction analysis. Then, the relationship between the levels of miR-138 and hypoxia-inducible factor (HIF)1-α was also investigated using a luciferase reporter assay. Assessment of myocardial infarct size, measurements of serum myocardial enzymes and electron microscopy analysis were all utilized to analyse the effect of miR-138 on myocardial I/R injury. The authors of current study also used western blotting to examine the expression levels of the mitochondrial fission-related proteins dynamin-1-like protein and mitochondrial fission 1 protein. It was found that miR-138 is downregulated and HIF1-α is upregulated after myocardial ischemia reperfusion injury. Overexpression of miR-138 reduced myocardial I/R injury-induced infarct sizes and myocardial enzyme levels, and it also inhibited the expression of proteins related to mitochondrial morphology and myocardial I/R-induced mitochondrial apoptosis by targeting HIF1-α. Taken together, these findings provide a novel insight into the molecular mechanism of miR-138 and HIF1-α in the progression of myocardial I/R injury. miR-138 has the potential to become a promising therapeutic target for treating myocardial I/R injury.