Pierre Flandin
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Pierre Flandin has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
Constance Barazzone-Argiroffo
1 shared publicationPatrick Muzzin
1 shared publicationYves Donati
1 shared publication
Latest Publications
- 23 May 2005
- Published by Wiley in FEBS Letters
- Vol. 579 (16) , 3411-3415
Hyperoxia‐mediated oxidative stress increases expression of UCP3 mRNA and protein in skeletal muscle
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.
- 23 May 2005
- Published by Wiley in FEBS Letters
- Vol. 579 (16) , 3411-3415
Hyperoxia‐mediated oxidative stress increases expression of UCP3 mRNA and protein in skeletal muscle
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.