期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 113, 期 1, 页码 114-123出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00431.2011
关键词
muscle atrophy; MuRF; atrogin; oxidative stress
资金
- Korea Science and Engineering Foundation (KOSEF)
- Korean government [2010-0007389]
- National Research Foundation of Korea [2010-0007389] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Bae S-K, Cha H-N, Ju T-J, Kim Y-W, Kim HS, Kim Y-D, Dan J-M, Kim J-Y, Kim S-d, Park S-Y. Deficiency of inducible nitric oxide synthase attenuates immobilization-induced skeletal muscle atrophy in mice. J Appl Physiol 113: 114-123, 2012. First published April 19, 2012; doi:10.1152/japplphysiol.00431.2011.-The present study examined the effects of inducible nitric oxide synthase (iNOS) deficiency on skeletal muscle atrophy in single leg-immobilized iNOS knockout (KO) and wild-type (WT) mice. The left leg was immobilized for 1 wk, and the right leg was used as the control. Muscle weight and contraction-stimulated glucose uptake were reduced by immobilization in WT mice, which was accompanied with increased iNOS expression in skeletal muscle. Deficiency of iNOS attenuated muscle weight loss and the reduction in contraction-stimulated glucose uptake by immobilization. Phosphorylation of Akt, mTOR, and p70S6K was reduced to a similar extent by immobilization in both WT and iNOS KO mice. Immobilization decreased FoxO1 phosphorylation and increased mRNA and protein levels of MuRF1 and atrogin-1 in WT mice, which were attenuated in iNOS KO mice. Aconitase and superoxide dismutase activities were reduced by immobilization in WT mice, and deficiency of iNOS normalized these enzyme activities. Increased nitrotyrosine and carbonylated protein levels by immobilization in WT mice were reversed in iNOS KO mice. Phosphorylation of ERK and p38 was increased by immobilization in WT mice, which was reduced in iNOS KO mice. Immobilization-induced muscle atrophy was also attenuated by an iNOS-specific inhibitor N-6-(1-iminoethyl)-L-lysine, and this finding was accompanied by increased FoxO1 phosphorylation and reduced MuRF1 and atrogin-1 levels. These results suggest that deficiency of iNOS attenuates immobilization-induced skeletal muscle atrophy through reduced oxidative stress, and iNOS-induced oxidative stress may be required for immobilization-induced skeletal muscle atrophy.
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