Li 2013 Free Radic Biol Med: Difference between revisions
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{{Publication | {{Publication | ||
|title=Li H, Kumar Sharma L, Li Y, Hu P, Idowu A, Liu | |title=Li H, Kumar Sharma L, Li Y, Hu P, Idowu A, Liu Danhui, Lu J, Bai Y (2013) Comparative bioenergetic study of neuronal and muscle mitochondria during aging. Free Radic Biol Med 63:30-40. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/23643721 PMID:23643721 Open Access] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/23643721 PMID:23643721 Open Access] | ||
|authors=Li | |authors=Li Hongzhi, Kumar Sharma Lokendra, Li Youfen, Hu Peiqing, Idowu Abimbola, Liu Danhui, Lu Jianxin, Bai Yidong | ||
|year=2013 | |year=2013 | ||
|journal=Free Radic Biol Med | |journal=Free Radic Biol Med | ||
|abstract=Mitochondrial respiratory chain defects have been associated with various diseases and with normal aging, particularly in tissues with high energy demands, including brain and skeletal muscle. Tissue-specific manifestation of mitochondrial DNA (mtDNA) mutations and mitochondrial dysfunction are hallmarks of mitochondrial diseases although the underlying mechanisms are largely unclear. Previously, we and others have established approaches for transferring mtDNA from muscle and synaptosomes of mice at various ages to cell cultures. In this study, we carried out a comprehensive bioenergetic analysis of cells bearing mitochondria derived from young, middle-aged, and old mouse skeletal muscles and synaptosomes. Significant age-associated alterations in oxidative phosphorylation and regulation during aging were observed in cybrids carrying mitochondria from both skeletal muscle and synaptosomes. Our results also revealed that loss of oxidative phosphorylation capacity may occur at various ages in muscle and brain. These findings indicate the existence of a tissue-specific regulatory mechanism for oxidative phosphorylation. | |abstract=Mitochondrial respiratory chain defects have been associated with various diseases and with normal aging, particularly in tissues with high energy demands, including brain and skeletal muscle. Tissue-specific manifestation of mitochondrial DNA (mtDNA) mutations and mitochondrial dysfunction are hallmarks of mitochondrial diseases although the underlying mechanisms are largely unclear. Previously, we and others have established approaches for transferring mtDNA from muscle and synaptosomes of mice at various ages to cell cultures. In this study, we carried out a comprehensive bioenergetic analysis of cells bearing mitochondria derived from young, middle-aged, and old mouse skeletal muscles and synaptosomes. Significant age-associated alterations in oxidative phosphorylation and regulation during aging were observed in cybrids carrying mitochondria from both skeletal muscle and synaptosomes. Our results also revealed that loss of oxidative phosphorylation capacity may occur at various ages in muscle and brain. These findings indicate the existence of a tissue-specific regulatory mechanism for oxidative phosphorylation. | ||
|keywords=Aging, Cybrid, Free radicals, Mitochondria, Skeletal muscle, Synaptosome | |keywords=Aging, Cybrid, Free radicals, Mitochondria, Skeletal muscle, Synaptosome | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, mt-Medicine, mt-Awareness | |area=Respiration, mt-Medicine, mt-Awareness | ||
|diseases=Aging;senescence | |||
|organism=Mouse | |organism=Mouse | ||
|tissues=Skeletal muscle, Nervous system | |tissues=Skeletal muscle, Nervous system | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|couplingstates=LEAK, ET | |||
|couplingstates=LEAK, | |pathways=N, S, CIV | ||
| | |||
}} | }} |
Latest revision as of 18:51, 29 February 2020
Li H, Kumar Sharma L, Li Y, Hu P, Idowu A, Liu Danhui, Lu J, Bai Y (2013) Comparative bioenergetic study of neuronal and muscle mitochondria during aging. Free Radic Biol Med 63:30-40. |
Li Hongzhi, Kumar Sharma Lokendra, Li Youfen, Hu Peiqing, Idowu Abimbola, Liu Danhui, Lu Jianxin, Bai Yidong (2013) Free Radic Biol Med
Abstract: Mitochondrial respiratory chain defects have been associated with various diseases and with normal aging, particularly in tissues with high energy demands, including brain and skeletal muscle. Tissue-specific manifestation of mitochondrial DNA (mtDNA) mutations and mitochondrial dysfunction are hallmarks of mitochondrial diseases although the underlying mechanisms are largely unclear. Previously, we and others have established approaches for transferring mtDNA from muscle and synaptosomes of mice at various ages to cell cultures. In this study, we carried out a comprehensive bioenergetic analysis of cells bearing mitochondria derived from young, middle-aged, and old mouse skeletal muscles and synaptosomes. Significant age-associated alterations in oxidative phosphorylation and regulation during aging were observed in cybrids carrying mitochondria from both skeletal muscle and synaptosomes. Our results also revealed that loss of oxidative phosphorylation capacity may occur at various ages in muscle and brain. These findings indicate the existence of a tissue-specific regulatory mechanism for oxidative phosphorylation. โข Keywords: Aging, Cybrid, Free radicals, Mitochondria, Skeletal muscle, Synaptosome
Labels: MiParea: Respiration, mt-Medicine, mt-Awareness
Pathology: Aging;senescence
Organism: Mouse Tissue;cell: Skeletal muscle, Nervous system Preparation: Intact cells
Coupling state: LEAK, ET
Pathway: N, S, CIV