Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

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

Zhanling Liao¹, Xiaoli Cheng², Chunyan Xiang³, Feng Liu¹

¹Department of CardiologyÃ¯Â¼Å’Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou City, Jiangsu Province 215028; ²Department of Cardiology, Shengjing Hospital Affiliated to China Medical University, Shenyang City, Liaoning Province 110004; ³Department of Cardiology, Dongying People's Hospital, Dongying City, Shandong Province 257000, China.

For correspondence:- Feng Liu Email: FengLiudfr@163.com Tel:+8651262629305

Accepted: 26 February 2020 Published: 31 March 2020

Citation: Liao Z, Cheng X, Xiang C, Liu F. MiR-138 ameliorates myocardial ischemia/reperfusion injury by targeting intercellular cell adhesion molecule 1. Trop J Pharm Res 2020; 19(3):489-495 doi: 10.4314/tjpr.v19i3.5

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

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 miR-138. 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.

Keywords: Intercellular cell adhesion molecule 1, MicroRNA-138, Myocardial/ischemia reperfusion injury, Reactive oxygen species