PMID- 25485704
OWN - NLM
STAT- MEDLINE
DCOM- 20150310
LR  - 20211203
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 456
IP  - 1
DP  - 2015 Jan 2
TI  - A treadmill exercise reactivates the signaling of the mammalian target of 
      rapamycin (mTor) in the skeletal muscles of starved mice.
PG  - 519-26
LID - S0006-291X(14)02160-3 [pii]
LID - 10.1016/j.bbrc.2014.11.118 [doi]
AB  - 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 24h 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 
      (12m/min, 2h, 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.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Zheng, Dong-Mei
AU  - Zheng DM
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan.
FAU - Bian, Zehua
AU  - Bian Z
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan.
FAU - Furuya, Norihiko
AU  - Furuya N
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan.
FAU - Oliva Trejo, Juan Alejandro
AU  - Oliva Trejo JA
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan.
FAU - Takeda-Ezaki, Mitsue
AU  - Takeda-Ezaki M
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan.
FAU - Takahashi, Katsuyuki
AU  - Takahashi K
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan.
FAU - Hiraoka, Yuka
AU  - Hiraoka Y
AD  - Laboratory of Proteomics and Biomolecular Science, Research Support Center, 
      Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
FAU - Mineki, Reiko
AU  - Mineki R
AD  - Laboratory of Proteomics and Biomolecular Science, Research Support Center, 
      Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
FAU - Taka, Hikari
AU  - Taka H
AD  - Laboratory of Proteomics and Biomolecular Science, Research Support Center, 
      Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
FAU - Ikeda, Shin-Ichi
AU  - Ikeda S
AD  - Sportology Center, Juntendo University Graduate School of Medicine, Tokyo 
      113-8421, Japan.
FAU - Komatsu, Masaaki
AU  - Komatsu M
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan; Protein Metabolism Project, Tokyo Metropolitan Institute of 
      Medical Science, Tokyo 156-8506, Japan.
FAU - Fujimura, Tsutomu
AU  - Fujimura T
AD  - Laboratory of Proteomics and Biomolecular Science, Research Support Center, 
      Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
FAU - Ueno, Takashi
AU  - Ueno T
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan; Laboratory of Proteomics and Biomolecular Science, Research 
      Support Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, 
      Japan.
FAU - Ezaki, Junji
AU  - Ezaki J
AD  - Department of Biochemistry, Juntendo University School of Medicine, Tokyo 
      113-8421, Japan; Translational Research Center, Fukushima Medical University, 
      Fukushima 960-1295, Japan. Electronic address: jezaki@fmu.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141206
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Map1lc3b protein, mouse)
RN  - 0 (Microtubule-Associated Proteins)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (Ribosomal Protein S6 Kinases)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Autophagy
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Microtubule-Associated Proteins/metabolism
MH  - Muscle, Skeletal/metabolism
MH  - Phosphorylation
MH  - *Physical Conditioning, Animal
MH  - Ribosomal Protein S6 Kinases/metabolism
MH  - Running
MH  - Signal Transduction
MH  - Starvation
MH  - TOR Serine-Threonine Kinases/*metabolism
OTO - NOTNLM
OT  - Autophagy
OT  - Exercise
OT  - GFP-LC3
OT  - Skeletal muscle
OT  - Treadmill
OT  - mTor
EDAT- 2014/12/09 06:00
MHDA- 2015/03/11 06:00
CRDT- 2014/12/09 06:00
PHST- 2014/11/25 00:00 [received]
PHST- 2014/11/28 00:00 [accepted]
PHST- 2014/12/09 06:00 [entrez]
PHST- 2014/12/09 06:00 [pubmed]
PHST- 2015/03/11 06:00 [medline]
AID - S0006-291X(14)02160-3 [pii]
AID - 10.1016/j.bbrc.2014.11.118 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2015 Jan 2;456(1):519-26. doi: 
      10.1016/j.bbrc.2014.11.118. Epub 2014 Dec 6.