MicroRNA-27a-3p Participates in the Myocardial Ischemia-Reperfusion Injury by Targeting Solute Carrier Family 7 Member 11 to Regulate Ferroptosis

Abstract

Background: Myocardial ischemia-reperfusion injury (MIRI) is usually accompanied by oxidative stress and inflammation, causing apoptosis. This study aimed to elucidate the regulatory function of microRNA (miRNA) on MIRI. Methods: Ferroptosis was evaluated using flow cytometry assay and DCFH-DA (2’,7’-dichlorodihydrofluorescein diacetate) method. Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) assays were carried out to measure gene expressions. qRT-PCR was used to measure the expression of miR-27a-3p and Solute Carrier Family 7 Member 11 (SLC7A11). Dual-luciferase reporter assay was performed to determine the targeting relationship between miR-27a-3p and SLC7A11. Hemotoxylin and eosin (H&E) staining and terminal deoxynucleoitidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining assays were conducted to visualize myocardial tissue injury. Results: Myocardial ischemia-reperfusion promoted cell apoptosis. Ferroptosis enhanced cell apoptosis and increased intracellular reactive oxygen species (ROS) and iron accumulation. The expression of miR-27a-3p was abnormally elevated after MIRI modeling, and SLC7A11 was a direct target of miR-27a-3p. Thus, by targeting SLC7A11, miR-27a-3p was found to regulate SLC7A11 expression negatively. Conclusions: In conclusion, miR-27a-3p was responsible for myocardial reperfusion injury in rats through sponging SLC7A11 to promote ferroptosis in cardiomyocytes.