Journal
LIFE SCIENCES
Volume 89, Issue 1-2, Pages 44-49Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2011.04.018
Keywords
Diabetes; Skeletal muscle atrophy; Oxidative stress; MuRF1
Funding
- Research Foundation of Education Department of Hubei Province, China [Q20104101]
Ask authors/readers for more resources
Aims: MuRF1 E3 ubiquitin ligase has been identified as a mediator of skeletal muscle wasting in various skeletal muscle atrophy models, and its expression is upregulated by oxidative stress. Exercise training could decrease oxidative stress and restore the atrophied skeletal muscle. Here, our aim was to investigate whether exercise training has any effect on MuRF1 expression in rats with diabetes. Main methods: Rats with streptozotocin-induced diabetes were subjected to exercise training, after which oxidative stress was determined, and MuRF1 expression was analyzed by immunohistochemistry, real-time RT-PCR and Western blot analysis. In addition, we analyzed C2C12 myotubes in an in vitro model to examine the effects of oxidative stress on the protein levels of MuRF1 and myosin heavy chain (MHC). Key findings: While oxidative stress and MuRF1 expression were increased in rats with diabetes, exercise training diminished the skeletal muscle wasting in diabetic rats by decreasing oxidative stress and inhibiting MuRF1 expression at both the mRNA and protein levels. In addition, oxidative stress-induced MuRF1 upregulation promoted proteasome dependent degradation of the myosin heavy chain (MHC) in C2C12 myotubes. Significance: Our study provides the first evidence that the beneficial anti-atrophy effects of exercise training on diabetes might be mediated by inhibiting oxidative stress-induced MuRF1 upregulation and preventing MuRF1-mediated degradation of MHC. (C) 2011 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available