Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10753732 | Biochemical and Biophysical Research Communications | 2015 | 8 Pages |
Abstract
It has been well established that a starvation-induced decrease in insulin/IGF-I and serum amino acids effectively suppresses the mammalian target of rapamycin (mTor) signaling to induce autophagy, which is a major degradative cellular pathway in skeletal muscles. In this study, we investigated the systematic effects of exercise on the mTor signaling of skeletal muscles. Wild type C57BL/6J mice were starved for 24Â h under synchronous autophagy induction conditions. Under these conditions, endogenous LC3-II increased, while both S6-kinse and S6 ribosomal protein were dephosphorylated in the skeletal muscles, which indicated mTor inactivation. Using GFP-LC3 transgenic mice, it was also confirmed that fluorescent GFP-LC3 dots in the skeletal muscles increased, including soleus, plantaris, and gastrocnemius, which clearly showed autophagosomal induction. These starved mice were then subjected to a single bout of running on a treadmill (12Â m/min, 2Â h, with a lean of 10 degrees). Surprisingly, biochemical analyses revealed that the exercise elicited a decrease in the LC3-II/LC3-I ratio as well as an inversion from the dephosphorylated state to the rephosphorylated state of S6-kinase and ribosomal S6 in these skeletal muscles. Consistently, the GFP-LC3 dots of the skeletal muscles were diminished immediately after the exercise. These results indicated that exercise suppressed starvation-induced autophagy through a reactivation of mTor signaling in the skeletal muscles of these starved mice.
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Authors
Dong-Mei Zheng, Zehua Bian, Norihiko Furuya, Juan Alejandro Oliva Trejo, Mitsue Takeda-Ezaki, Katsuyuki Takahashi, Yuka Hiraoka, Reiko Mineki, Hikari Taka, Shin-ichi Ikeda, Masaaki Komatsu, Tsutomu Fujimura, Takashi Ueno, Junji Ezaki,