| Exercise increases mitochondrial PGC-1alpha content and promotes nuclear-mitochondrial cross-talk to coordinate mitochondrial biogenesis. | |
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MedLine Citation:
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PMID: 21245132 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Endurance exercise is known to induce metabolic adaptations in skeletal muscle via activation of the transcriptional co-activator peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α). PGC-1α regulates mitochondrial biogenesis via regulating transcription of nuclear-encoded mitochondrial genes. Recently, PGC-1α has been shown to reside in mitochondria; however, the physiological consequences of mitochondrial PGC-1α remain unknown. We sought to delineate if an acute bout of endurance exercise can mediate an increase in mitochondrial PGC-1α content where it may co-activate mitochondrial transcription factor A to promote mtDNA transcription. C57Bl/6J mice (n = 12/group; ♀ = ♂) were randomly assigned to sedentary (SED), forced-endurance (END) exercise (15 m/min for 90 min), or forced endurance +3 h of recovery (END+3h) group. The END group was sacrificed immediately after exercise, whereas the SED and END+3h groups were euthanized 3 h after acute exercise. Acute exercise coordinately increased the mRNA expression of nuclear and mitochondrial DNA-encoded mitochondrial transcripts. Nuclear and mitochondrial abundance of PGC-1α in END and END+3h groups was significantly higher versus SED mice. In mitochondria, PGC-1α is in a complex with mitochondrial transcription factor A at mtDNA D-loop, and this interaction was positively modulated by exercise, similar to the increased binding of PGC-1α at the NRF-1 promoter. We conclude that in response to acute altered energy demands, PGC-1α re-localizes into nuclear and mitochondrial compartments where it functions as a transcriptional co-activator for both nuclear and mitochondrial DNA transcription factors. These results suggest that PGC-1α may dynamically facilitate nuclear-mitochondrial DNA cross-talk to promote net mitochondrial biogenesis. |
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Authors:
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Adeel Safdar; Jonathan P Little; Andrew J Stokl; Bart P Hettinga; Mahmood Akhtar; Mark A Tarnopolsky |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-01-18 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 286 ISSN: 1083-351X ISO Abbreviation: J. Biol. Chem. Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-04-01 Completed Date: 2011-06-09 Revised Date: 2012-03-26 |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 10605-17 Citation Subset: IM |
Affiliation:
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Department of Kinesiology, McMaster University, Hamilton, Ontario L8N 3Z5, Canada. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Nucleus / genetics, metabolism* DNA, Mitochondrial / genetics, metabolism DNA-Binding Proteins / genetics, metabolism Energy Metabolism / physiology* Female Male Mice Mitochondria, Muscle / genetics, metabolism* Mitochondrial Proteins / genetics, metabolism Nuclear Respiratory Factor 1 / biosynthesis, genetics Physical Conditioning, Animal* Physical Endurance / physiology Promoter Regions, Genetic / physiology Trans-Activators / biosynthesis*, genetics Transcription Factors / genetics, metabolism Transcription, Genetic / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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MOP97805//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/DNA, Mitochondrial; 0/DNA-Binding Proteins; 0/Mitochondrial Proteins; 0/Nrf1 protein, mouse; 0/Nuclear Respiratory Factor 1; 0/Ppargc1a protein, mouse; 0/Trans-Activators; 0/Transcription Factors; 0/mitochondrial transcription factor A |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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