Abstract
A functional role of superoxide dismutase 3 in nitric oxide‐mediated protection against catabolic wasting in skeletal muscle
The FASEB journal, Vol.24(S1), pp.lb672-lb672
04/2010
DOI: 10.1096/fasebj.24.1_supplement.lb672
Abstract
Oxidative myofibers are resistant to catabolic wasting caused by many chronic diseases, such as congestive heart failure and sepsis. We have recently identified a nitric oxide‐dependent antioxidant defense mechanism in this oxidative phenotype‐associated protection. Here, we show that systemic administration of NO donor GSNO (4 mg/kg/day, i.p.) significantly suppressed glucocorticoid‐induced (dexamethasone, 25 mg/kg/day, i.p.) loss of muscle mass and increases in E3 ligases MAFbx/atrogin‐1 mRNA expression in glyocolytic muscles. GSNO also prevented dexamethasone‐induced reduction of superoxide dismutase 3 (SOD3) protein expression. Importantly, somatic gene transfer of SOD3 in glycolytic tibialis anterior muscle significantly attenuated dexamethasone‐induced muscle atrophy. These findings suggest the functional importance of SOD3 in NO‐mediated protection against catabolic wasting in skeletal muscle.
Details
- Title: Subtitle
- A functional role of superoxide dismutase 3 in nitric oxide‐mediated protection against catabolic wasting in skeletal muscle
- Creators
- Mitsuharu Okutsu - University of VirginiaVitor A Lira - University of VirginiaMei Zhang - University of VirginiaZhen Yan - University of Virginia
- Resource Type
- Abstract
- Publication Details
- The FASEB journal, Vol.24(S1), pp.lb672-lb672
- Publisher
- Federation of American Societies for Experimental Biology
- DOI
- 10.1096/fasebj.24.1_supplement.lb672
- ISSN
- 0892-6638
- eISSN
- 1530-6860
- Number of pages
- 1
- Language
- English
- Date published
- 04/2010
- Academic Unit
- Health and Human Physiology
- Record Identifier
- 9984267142502771
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