2013 Fiscal Year Annual Research Report
有酸素運動によるオートファジー抑制メカニズムの解明
| Project/Area Number |
24700705
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| Research Institution | Juntendo University |
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Principal Investigator |
鄭 冬梅 順天堂大学, 医学(系)研究科(研究院), 非常勤助教 (10420829)
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| Keywords | autophagy / endurance exercise / muscle / mTOR / LC3 / treadmill |
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| Research Abstract |
It has been well established that starvation-induced decrease in insulin/IGF-I and serum amino acids effectively suppresses the mammalian target of rapamycin (mTor) signaling to induce autophagy, a cellular major degradative pathway, in skeletal muscles. In this study, I investigated effect of treadmill running exercise on mTor signaling of skeletal muscles. In starved GFP-LC3 transgenic mice, both S6-kinse and ribosomal subunit S6 were dephosphorylated in the skeletal muscles, including soleus, plantaris, gastrocnemius, and extensor digitorum longus. Simultaneously, fluorescent GFP-LC3 dots increased, clearly showing autophagosomal induction under mTor inactivation. These starved mice were then subjected to single-bout of running exercise using a treadmill (12 m/min, 2 hr, with a lean of 10 degrees). Surprisingly, the GFP-LC3 dots of skeletal muscles were dissipated immediately after treadmill exercise. Furthermore, biochemical analyses revealed that the exercise elicited decrease in LC3-II/LC3-I ratio as well as the inversion from dephosphorylated state to rephosphorylated state of S6-kinase and ribosomal S6 in these skeletal muscles. These results indicate that treadmill-running exercise represses starvation-induced autophagy by reactivation of mTor signaling in the skeletal muscles of starved mice.
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