Abstract

The activation of Janus Kinase(JAK)/ signal transducers and activators of transcription(STAT) pathway has been reported to induce cardiac hypertrophy in genetically hypertensive and experimental post-myocardial infarction rats, as well as in isolated ventricular myocytes subject to mechanical stretch. Our previous study showed that acute exercise induced JAK/STAT pathway activation; however, no reports have documented the activation of JAK/STAT pathway in the myocardium of exercise-induced cardiac hypertrophy. PURPOSE: To evaluate endurance training on JAK/STAT3 pathway and Suppressor of cytokine signaling (SOCS) expression in myocardium in order to understand the mechanism of JAK/STAT3 pathway in exercise induced cardiac hypertrophy. METHODS: Male Sprague-Dawley rats(220±5g) were randomly divided into sedentary and exercise groups, rats in exercise group were submitted to grade treadmill training for 10 weeks, then sacrificed at 0hour and 24 hours after last exercise respectively. phosphorylated (p) - STAT3, STAT3, JAK1, JAK3 and SOCS1, SOCS2,SOCS6 expression in left ventricle determined with either western blot or immunohistochemistry. RESULTS: The heart/body weight ratio of exercised rats significantly higher in comparison with the sedentary rats (p<0.05); the percentage of JAK1 positive cells significantly increased immediately after the last running in exercised rats(p<0.01); however, the percentage of JAK3 positive cells showed no change either immediately or 24 hours after last exercise (p>0.05); p-STAT3/STAT3 ratio increased immediately after last exercise (p<0.05); while the percentage of SOCS1 and SOCS2 positive cells increased remarkably both immediately (p<0.01, p<0.05) and 24 hours (p<0.05) after last exercise, while SOCS6 expression showed no changes in exercised groups compared with the sedentary group(p>0.05). CONCLUSIONS: Exercise training that induced activation of JAK/STAT3 pathway might be related to the exercise-induced cardiac hypertrophy, the different responses of JAK1 and JAK3 might indicate the different functions of JAKs in exercised heart and the expression changes of SOCS1 and SOCS2 might be involved in regulating JAK/STAT3 signal pathway in exercised-induced cardiac hypertrophy.

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