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: 3.58). 07/2005; 579(16):3411-5. DOI: 10.1016/j.febslet.2005.04.084
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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