ABSTRACT

　 Regular exercise improves mitochondrial quality and quantity that contribute to maintain skeletal muscle homeostasis. Mitophagy, a mitochondrial quality control system by degradation of dysfunctional or superfluous mitochondria, is a major mechanism to maintain mitochondrial quality and quantity. Autophagy adaptor protein, p62/SQSTM1, regulates mitophagy and exercise increases p62 and phosphorylated p62 protein in muscle. However, role of p62 to control mitophagy in skeletal muscle is not well understood. In this study, we hypothesized that phosphorylated p62 induces mitophagy in skeletal muscle and contribute to maintain muscle homeostasis. Here, we demonstrated that regular exercise increases autophagy and mitophagy protein expression in oxidative soleus muscle. These autophagy and mitophagy protein expression in muscle specific-p62 knockout mice were consistent with the wild-type littermate mice. Muscle specific-p62 transgenic mice inhibited LC3-I and Pink1 proteins, on the other hand, increased Binip3 protein expression in compare to the wildtype littermate mice. These results suggest that p62 phosphorylation by gene transfer induces mitophagy but not exercise-induced p62 phosphorylation in oxidative soleus muscle.

DECENTE SPORTS SCIENCE Vol.43/The DESCENTE AND ISHIMOTO MEMORIAL FOUNDATION FOR THE PROMOTION SPORTS SCIENCE