Article

Hyperoxia-mediated oxidative stress increases expression of UCP3 mRNA and protein in skeletal muscle.

Department of Cell Physiology and Metabolism, Centre Médical Universitaire, 1 rue Michel Servet, 1211 Geneva 4, Switzerland.
FEBS Letters (impact factor: 3.54). 07/2005; 579(16):3411-5. DOI:10.1016/j.febslet.2005.04.084 pp.3411-5
Source: PubMed

ABSTRACT The uncoupling protein-3 (UCP3) is a mitochondrial protein expressed mainly in skeletal muscle. Among several hypotheses for its physiological function, UCP3 has been proposed to prevent excessive production of reactive oxygen species. In the present study, we evaluated the effect of an oxidative stress induced by hyperoxia on UCP3 expression in mouse skeletal muscle and C2C12 myotubes. We found that the hyperoxia-mediated oxidative stress was associated with a 5-fold and 3-fold increase of UCP3 mRNA and protein levels, respectively, in mouse muscle. Hyperoxia also enhanced reactive oxygen species production and UCP3 mRNA expression in C2C12 myotubes. Our findings support the view that both in vivo and in vitro UCP3 may modulate reactive oxygen species production in response to an oxidative stress.

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Keywords

3-fold increase
 
C2C12 myotubes
 
excessive production
 
findings support
 
hyperoxia
 
hyperoxia-mediated oxidative stress
 
hypotheses
 
mitochondrial protein
 
mouse skeletal muscle
 
oxidative stress
 
oxidative stress induced
 
physiological function
 
protein levels
 
skeletal muscle
 
UCP3
 
UCP3 expression
 
UCP3 mRNA
 
UCP3 mRNA expression
 
uncoupling protein-3
 
vitro UCP3
 

Pierre Flandin