Difference between revisions of "Takahashi 2014 Exp Gerontol"
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{{Publication | {{Publication | ||
|title=Takahashi K, Noda Y, Ohsawa I, Shirasawa T, Takahashi M (2014) Extended lifespan, reduced body size and leg skeletal muscle mass, and decreased mitochondrial function in clk-1 transgenic mice. Exp Gerontol [Epub ahead of print]. Β | |title=Takahashi K, Noda Y, Ohsawa I, Shirasawa T, Takahashi M (2014) Extended lifespan, reduced body size and leg skeletal muscle mass, and decreased mitochondrial function in clk-1 transgenic mice. Exp Gerontol [Epub ahead of print]. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25106098 PMID: 25106098] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/25106098 PMID: 25106098] | ||
|authors=Takahashi K, Noda Y, Ohsawa I, Shirasawa T, Takahashi M | |authors=Takahashi K, Noda Y, Ohsawa I, Shirasawa T, Takahashi M | ||
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|organism=Mouse | |organism=Mouse | ||
|tissues=Skeletal muscle, Liver | |tissues=Skeletal muscle, Liver | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|diseases=Aging; senescence | |diseases=Aging;senescence | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
|substratestates=CI, CI | |substratestates=CI, CI&II | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Revision as of 16:15, 10 February 2015
Takahashi K, Noda Y, Ohsawa I, Shirasawa T, Takahashi M (2014) Extended lifespan, reduced body size and leg skeletal muscle mass, and decreased mitochondrial function in clk-1 transgenic mice. Exp Gerontol [Epub ahead of print]. |
Takahashi K, Noda Y, Ohsawa I, Shirasawa T, Takahashi M (2014) Exp Gerontol
Abstract: Mutational inactivation of clk-1, which encodes an enzyme necessary for the biosynthesis of coenzyme Q (CoQ), extends the lifespan of Caenorhabditis elegans. However, whether mammalian clk-1 regulates the lifespan of mice is not known because clk-1-deficiencies are embryonic lethal. Here, we investigated the lifespan of clk-1 transgenic mice (Tg96/I), which were rescued from embryonic lethality via the transgenic expression of mouse clk-1. Tg96/I mice lived longer and had smaller bodies than wild-type mice, but Tg96/I mice had CoQ levels equivalent to wild-type mice. The small-sized Tg96/I mice exhibited reduced whole-body oxygen consumption (VO2) during the dark period, and lean leg skeletal muscles with reduced mitochondrial VO2 and ATP content compared with wild-type mice. These findings indicate a close relationship between lifespan extension and decreased mitochondrial function, which was induced by the transgenic expression of clk-1, in leg skeletal muscles that exhibit high metabolic activity. β’ Keywords: Lifespan, Mitochondrial function, clk-1, Coenzyme Q, Oxygen consumption, Leg skeletal muscles
β’ O2k-Network Lab: JP Tokyo Tanaka M
Labels: MiParea: Respiration, Genetic knockout;overexpression, Gender
Pathology: Aging;senescence
Organism: Mouse Tissue;cell: Skeletal muscle, Liver Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k