Mitofusions1/2 and ERRα expression are increased in human skeletal muscle after physical exercise. Cartoni, Romain, Leger, Bertrand, Hock, M. Benjamin, Praz, Manu, Crettenand, Antoinette, Pich, Sara, Ziltener, Jean-Luc, Luthi, François, Deriaz, Olivier, Zorzano, Antonio, Gobelet, Charles, Kralli, Anastasia and Russell, Aaron 2005, Mitofusions1/2 and ERRα expression are increased in human skeletal muscle after physical exercise., Journal of physiology, vol. 567, no. 1, pp. 349-358, doi: 10.1113/jphysiol.2005.092031. Attached Files Name Description MIMEType Size Downloads Title Mitofusions1/2 and ERRα expression are increased in human skeletal muscle after physical exercise. Author(s) Cartoni, Romain Leger, Bertrand Hock, M. Benjamin Praz, Manu Crettenand, Antoinette Pich, Sara Ziltener, Jean-Luc Luthi, François Deriaz, Olivier Zorzano, Antonio Gobelet, Charles Kralli, Anastasia Russell, Aaron orcid.org/0000-0002-7323-9501 Journal name Journal of physiology Volume number 567 Issue number 1 Start page 349 End page 358 Publisher Cambridge University Press Place of publication London, England Publication date 2005 ISSN 0022-3751 1469-7793 Summary 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 COX IV 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. Language eng DOI 10.1113/jphysiol.2005.092031 Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences HERDC Research category C1.1 Refereed article in a scholarly journal Copyright notice ©2005, The Physiological Society Free to Read? Yes Persistent URL http://hdl.handle.net/10536/DRO/DU:30009131 Document type: Journal Article Collections: Faculty of Health School of Exercise and Nutrition Sciences Institute for Physical Activity and Nutrition Open Access Collection Related Links Link Description Link to full-text (open access)   Connect to published version (restricted access) Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au. Versions Version Filter Type Tue, 03 Feb 2009, 13:02:07 EST Fri, 14 May 2010, 12:20:50 EST Tue, 10 Dec 2013, 14:57:13 EST Mon, 16 Jun 2014, 09:59:34 EST Wed, 30 Sep 2020, 22:36:05 EST Filtered Full Citation counts:   Cited 270 times in TR Web of Science Cited 283 times in Scopus Search Google Scholar Access Statistics: 949 Abstract Views, 0 File Downloads  -  Detailed Statistics Created: Mon, 13 Oct 2008, 15:52:01 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.