Mitofusins 1/2 and ERRα expression are increased in human skeletal muscle after physical exercise

Romain Cartoni, Bertrand Léger, M. Benjamin Hock, Manu Praz, Antoinette Crettenand, Sara Pich, Jean Luc Ziltener, François Luthi, Olivier Dériaz, Antonio Zorzano, Charles Gobelet, Anastasia Kralli, Aaron P. Russell

Research output: Contribution to journalArticlepeer-review

Abstract

Mitochondrial impairment is hypothesized to contribute to the pathogenesis of insulin resistance. Mitofusin (Mfn) proteins regulate the biogenesis and maintenance of the mitochondrial network, and when inactivated, cause a failure in the mitochondrial architecture and decreases in oxidative capacity and glucose oxidation. Exercise increases muscle mitochondrial content, size, oxidative capacity and aerobic glucose oxidation. To address if Mfn proteins are implicated in these exercise-induced responses, we measured Mfn1 and Mfn2 mRNA levels, pre-, post-, 2 and 24 h post-exercise. Additionally, we measured the expression levels of transcriptional regulators that control mitochondrial biogenesis and functions, including PGC-1α, NRF-1, NRF-2 and the recently implicated ERRα. We show that Mfn1, Mfn2, NRF-2 and COXIV mRNA were increased 24 h post-exercise, while PGC-1α and ERRα mRNA increased 2 h post-exercise. Finally, using in vitro cellular assays, we demonstrate that Mfn2 gene expression is driven by a PGC-1α programme dependent on ERRα. The PGC-1α/ERRα-mediated induction of Mfn2 suggests a role of these two factors in mitochondrial fusion. Our results provide evidence that PGC-1α not only mediates the increased expression of oxidative phosphorylation genes but also mediates alterations in mitochondrial architecture in response to aerobic exercise in humans.

Original languageEnglish (US)
Pages (from-to)349-358
Number of pages10
JournalJournal of Physiology
Volume567
Issue number1
DOIs
StatePublished - Aug 15 2005
Externally publishedYes

ASJC Scopus subject areas

  • Physiology

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