Downregulation of OIP5-AS1 inhibits apoptosis in myocardial ischemia/reperfusion injury via modulating the MiR-145-5p/ROCK1 axis

• Published in: PloS one Vol. 20; no. 5; p. e0324909
• Main Authors: Yang, Jingyan, Liu, Jing, Liu, Xiaobo, Xu, Dongling, Zhang, Juan
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 20.05.2025; Public Library of Science (PLoS)
• Subjects: Analysis; Animal models; Animals; Antisense RNA; Apoptosis; Apoptosis - genetics; BAX protein; Bcl-2 protein; Binding sites; Biology and Life Sciences; Carbon dioxide; Cardiomyocytes; Cardiomyopathy; Care and treatment; Caspase-3; Cell Line; Complications and side effects; Coronary artery; Cytotoxicity; Depletion; Diagnosis; Down-Regulation; Gene therapy; Health aspects; Heart diseases; Hypoxia; Injury prevention; Ischemia; Kinases; Laboratory animals; Male; Medicine and Health Sciences; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; miRNA; Myocardial ischemia; Myocardial Reperfusion Injury - genetics; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - pathology; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Ostomy; Patient outcomes; Plasmids; Proteins; Rats; Rats, Sprague-Dawley; Reperfusion; Reperfusion injury; Research and Analysis Methods; rho-Associated Kinases - genetics; rho-Associated Kinases - metabolism; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Signal Transduction; China; United States > US
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0324909

The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms. In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined. Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions. Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis.