MRNA and protein expression of sarcKATP channel subunit Kir6.2 after exercise-induced myocardial injury in rats.

Abstract

To investigate the expression of kir6.2 subunit of the sarcKATP channel in exercise-induced myocardial injury and to elucidate the underlying mechanism of myocardial protection by sarcKATP channels. Healthy male Sprague Dawley(SD) rats were divided into the Control (C) and the Exhaustive Exercise (EE) group. The one-time exhaustive exercise-induced myocardial injury model was established on a treadmill at a speed of 35 m/min. Alterations in myocardial ischemia and hypoxia were examined by hematoxylin-basic fuchsin-picric acid (HBFP) staining and the concentration of cardiac Troponin I (cTnl), a sensitive and specific marker for myocardial injury, was detected using immunochemiluminescence analysis. The mRNA expression level, localization, and protein expression of sarcKATP channel subunit kir6.2 were determined by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), immunofluorescence, and Western blot analysis, respectively. When compared to Group C, rats in Group EE demonstrated significantly increased areas of myocardial ischemia and hypoxia. Moreover, increased serum levels of cTnI were detected. Increased kir6.2 expression was found on the surface of cardiomyocytes and kir6.2 protein expression was also significantly increased. Exercise-induced myocardial injury did not result in noticeable alterations in kir6.2 mRNA expression. However, kir6.2 protein expression was significantly increased and resulted in increased numbers of sarcKATP channel openings in the myocardium, thereby further inhibiting exercise-induced myocardial injury.