Deficiency of inducible nitric oxide synthase attenuates immobilization-induced skeletal muscle atrophy in mice

Title
Deficiency of inducible nitric oxide synthase attenuates immobilization-induced skeletal muscle atrophy in mice
Author(s)
배상근[배상근]차혜나주태진김용운김희선김용대단진명[단진명]김종연김세동박소영
Keywords
STIMULATED GLUCOSE-UPTAKE; OXIDATIVE STRESS; PHYSIOLOGICAL FUNCTIONS; SIGNALING PATHWAYS; INSULIN-RESISTANCE; UBIQUITIN LIGASES; PROTEIN-SYNTHESIS; UP-REGULATION; CONTRACTION; MECHANISMS
Issue Date
201207
Publisher
AMER PHYSIOLOGICAL SOC
Citation
JOURNAL OF APPLIED PHYSIOLOGY, v.113, no.1, pp.114 - 123
Abstract
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.
URI
http://hdl.handle.net/YU.REPOSITORY/27711http://dx.doi.org/10.1152/japplphysiol.00431.2011
ISSN
8750-7587
Appears in Collections:
중앙도서관 > rims journal
의과대학 > 생리학교실 > Articles
의과대학 > 미생물학교실 > Articles
의과대학 > 이비인후과학교실 > Articles
의과대학 > 정형외과학교실 > Articles
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE