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: 3.17). 07/2005; 579(16):3411-5. DOI: 10.1016/j.febslet.2005.04.084
Source: PubMed


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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Available from: Constance Barazzone-Argiroffo, May 20, 2015
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    • "Oxygen itself acts as a free radical [30], and a high oxygen tension is correlated with the production of ROS. Thus, detection of ROS implies the existence of oxidative stress [37] [38], and such oxidative stress is induced in proportion to the oxygen tension [36] [39] [40]. We confirmed that the hyperoxic culture medium had a 2-fold higher ROS content than the normoxic medium in our vitro study (data not shown). "

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    • "Proteomic analysis of C2C12 cells indicates that respiratory chain proteins are up-regulated by 10 days postdifferentiation (Kislinger et al. 2005), resulting in increased potential for generation of oxidative stress. This is countered, in part, by up-regulation of uncoupling protein-3 (Flandin et al. 2005). Given that these data illustrate the importance of managing the increased oxidative stress that can be generated by differentiated skeletal muscle, our data indicating residual telomerase activity in post-mitotic cells suggests a potential role for telomerase, independent of its role in maintaining telomeric structure. "

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    • "Furthermore, induction of both Ucp2 and Ucp3 has also been shown previously to be induced by β-AR signaling in exercising skeletal muscle [27,76-78]. Since Ucp3 and Ucp2 have been implicated in the reduction of ROS [79,80], it is possible that the induction of Ucp3 and Ucp2 expression in skeletal muscle is one mechanism for reducing ROS production during or after exercise. "
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