Inhibition of MicroRNA-206 Ameliorates Ischemia-Reperfusion Arrhythmia in a Mouse Model by Targeting Connexin43.

Abstract

Reperfusion arrhythmias (RA) are an important cause of sudden cardiac death and is closely associated with gap junction protein in the heart, connexin 43 (Cx43). This study is aimed at elucidating the molecular association between microRNA-206 (miR-206) and Cx43 in ischemia-reperfusion arrhythmia using experimental animal model. Our results showed that miR-206 inhibitor alleviated ischemia-reperfusion-induced arrhythmias, indicated by the lower extent of changes in heart rate (HR), PR interval, rate pressure product (RPP), and mean arterial pressure (MAP). miR-206 inhibitor also downregulated the serum creatine kinase isoenzyme (CKMB) and cardiac troponin I (cTnI) levels in mice under myocardial ischemia-reperfusion (IR) process. The knockdown of Cx43 inversed the protective effects of miR-206 inhibitor on cardiac arrhythmias. These results supported that inhibition of miR-206 ameliorates ischemia-reperfusion arrhythmia by targeting Cx43, and this miR-206/Cx43 axis could serve as a potential target for the management of ischemic-perfusion arrhythmia.