Takahashi 2014 Exp Gerontol

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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 58:146-53.

» PMID: 25106098

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.

Keywords: Lifespan, Mitochondrial function, clk-1, Coenzyme Q, Oxygen consumption, Leg skeletal muscles

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  Pathway: N, NS  HRR: Oxygraph-2k 

JP