PGC-1α is required for training-induced prevention of age-associated decline in mitochondrial enzymes in mouse skeletal muscle
PGC-1α is required for training-induced prevention of age-associated decline in mitochondrial enzymes in mouse skeletal muscle
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DOI：
10.1016/j.exger.2010.01.011
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发表时间：
2010-05-01
影响因子：
3.9
通讯作者：
Pilegaard, Henriette
中科院分区：
文献类型：
--
作者：
Leick, Lotte;Lyngby, Stine Secher;Pilegaard, Henriette
本研究的目的是检验运动训练通过 PGC-1 α 依赖性机制预防与年龄相关的骨骼肌线粒体酶下降的假设。全身 PGC-1 α 敲除 (KO) 和同窝野生型 (WT) 小鼠在 2 至 13 个月大时接受长期跑轮运动训练或久坐生活方式。此外，一组大约 4 个月大的小鼠被用作年轻的未经训练的对照组。在这两种基因型中，与年轻的未经训练的小鼠相比，13 个月大的未经训练的小鼠的柠檬酸合酶 (CS) 活性和超氧化物歧化酶 (SOD)2 蛋白含量均与年龄相关，降低了 30%。然而，训练仅在 WT 小鼠中阻止了与年龄相关的 CS 活性和 SOD2 蛋白含量的下降，但长期运动训练确实增加了两种基因型的 HKII 蛋白含量。此外，虽然 PGC-1 α 小鼠骨骼肌中 CS 活性以及 cytc 和 SOD2 蛋白表达比 WT 小鼠低 50-150%，但促凋亡蛋白 Bax 和抗凋亡 Bcl2 的表达与 PGC-1 α KO 小鼠中升高 30% 相似。总之，目前的研究结果表明，PGC-1 α 对于训练诱导的预防骨骼肌中 CS 活性和 SOD2 蛋白表达与年龄相关的下降是必需的。 (C) 2010 爱思唯尔公司保留所有权利
The aim of the present study was to test the hypothesis that exercise training prevents an age-associated decline in skeletal muscle mitochondrial enzymes through a PGC-1 alpha dependent mechanism Whole body PGC-1 alpha knock-out (KO) and littermate wildtype (WT) mice were submitted to long term running wheel exercise training or a sedentary lifestyle from 2 to 13 month of age. Furthermore, a group of approximately 4-month-old mice was used as young untrained controls. There was in both genotypes an age-associated similar to 30% decrease in citrate synthase (CS) activity and superoxide dismutase (SOD)2 protein content in 13-month-old untrained mice compared with young untrained mice. However, training prevented the age-associated decrease in CS activity and SOD2 protein content only in WT mice, but long term exercise training did increase HKII protein content in both genotypes. In addition, while CS activity and protein expression of cytc and SOD2 were 50-150% lower in skeletal muscle of PGC-1 alpha mice than WT mice, the expression of the pro-apoptotic protein Bax and the anti-apoptotic Bcl2 was similar to 30% elevated in PGC-1 alpha KO mice. In conclusion, the present findings indicate that PGC-1 alpha is required for training-induced prevention of an age-associated decline in CS activity and SOD2 protein expression in skeletal muscle. (C) 2010 Elsevier Inc All rights reserved