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Purpose: To explore the effect of miR-138 on regulating intercellular cell adhesion molecule 1 (ICAM-1) expression in endothelial cells to alleviate cardiac ischemia/reperfusion (I/R) injury and its related mechanisms. Methods: The left anterior descending artery of the heart was occluded for 30 min and then perfused for 2 h to induce a rat model of cardiac I/R injury. H9C2 cells were cultured in an anoxic medium without serum to establish the model of hypoxia/reoxygenation (H/R). Triphenyl tetrazolium chloride (TTC) staining was applied to measure myocardial infarction sizes in rat hearts. The mRNA expression levels of miR-138 and ICAM-1 were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). Dual luciferase reporter assay was used to identify the target of miR-138. The agomiR-138 and miR-138 mimics were transfected into H9C2 cells; exogenous ICAM-1 was also administered, and ROS accumulation, cell viability, and apoptosis were measured. Furthermore, the underlying mechanism was investigated. Results: MiR-138 was downregulated both in vitro and in vivo. AgomiR-138 reduced myocardial infarction area, decreased ROS production and suppressed cell apoptosis in a rat model of cardiac I/R injury. On the other hand, miR-138 mimics increased cell viability, enhanced ROS production and induced cell apoptosis in H/R-induced H9C2 cells. Further analysis verified ICAM-1 as a target of miR138. Besides, exogenous ICAM-1 inhibited the protective effect of miR-138 on H/R-induced apoptosis in vitro. Conclusion: MiR-138 may protect against injury of myocardial I/R by targeting ICAM-1. The results also provide insight into miR-138/ICAM-1 axis as new therapeutic targets for myocardial I/R injury.

MiR-138 ameliorates myocardial ischemia/reperfusion injury by targeting intercellular cell adhesion molecule 1