Journal of applied physiology (1985), 2012-07, Vol.113 (1), p.114-123
2012
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- Autor(en) / Beteiligte
- Titel
- Deficiency of inducible nitric oxide synthase attenuates immobilization-induced skeletal muscle atrophy in mice
- Ist Teil von
- Journal of applied physiology (1985), 2012-07, Vol.113 (1), p.114-123
- Ort / Verlag
- Bethesda, MD: American Physiological Society
- Erscheinungsjahr
- 2012
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 8750-7587eISSN: 1522-1601DOI: 10.1152/japplphysiol.00431.2011Titel-ID: cdi_proquest_miscellaneous_1023293541
- Format
- –
- Schlagworte
- Aconitate Hydratase - metabolism, Animals, Biological and medical sciences, Enzyme Inhibitors - pharmacology, Forkhead Box Protein O1, Forkhead Transcription Factors - metabolism, Fundamental and applied biological sciences. Psychology, Gene expression, Glucose - metabolism, Hindlimb Suspension, Lysine - analogs & derivatives, Lysine - pharmacology, Male, MAP Kinase Signaling System - drug effects, Mice, Mice, Knockout, Muscle Contraction - drug effects, Muscle Contraction - physiology, Muscle Proteins - metabolism, Muscle, Skeletal - anatomy & histology, Muscle, Skeletal - enzymology, Muscular Atrophy - enzymology, Musculoskeletal system, Nitric oxide, Nitric Oxide Synthase Type II - deficiency, Nitric Oxide Synthase Type II - genetics, Phosphorylation, Physiology, Protein Carbonylation - physiology, Proteins, Proto-Oncogene Proteins c-akt - metabolism, Ribosomal Protein S6 Kinases, 70-kDa - metabolism, Rodents, SKP Cullin F-Box Protein Ligases - metabolism, Superoxide Dismutase - metabolism, TOR Serine-Threonine Kinases - metabolism, Tripartite Motif Proteins, Tyrosine - analogs & derivatives, Tyrosine - analysis, Ubiquitin-Protein Ligases - metabolism