Chronic Exercise Training Improved Aortic Endothelial and Mitochondrial Function via an AMPKα2-Dependent Manner.
Chronic Exercise Training Improved Aortic Endothelial and Mitochondrial Function via an AMPKα2-Dependent Manner.
复制标题
慢性运动训练通过 AMPKalpha2 依赖性方式改善主动脉内皮和线粒体功能。
DOI：
10.3389/fphys.2016.00631
复制
发表时间：
2016
影响因子：
4
通讯作者：
Gao P
中科院分区：
文献类型：
--
作者：
Chen X;An X;Chen D;Ye M;Shen W;Han W;Zhang Y;Gao P
慢性运动训练已知可保护血管；然而，其潜在机制仍不清楚。本研究假设运动可能通过一种依赖腺苷酸活化蛋白激酶α2（AMPKα2）的方式改善主动脉内皮和线粒体功能。10周龄的AMPKα2基因敲除（AMPKα2 - / -）小鼠和年龄匹配的野生型（WT）小鼠进行每日跑步机跑步，持续6周，然后取这些小鼠的胸主动脉用于进一步检测。我们的结果显示，运动显著促进了野生型小鼠的血管舒张，增加了内皮型一氧化氮合酶（eNOS）的表达和磷酸化，同时AMPKα2的表达也增加。在AMPKα2 - / -小鼠中未观察到这些效应。此外，运动训练增加了野生型小鼠胸主动脉线粒体含量，表现为复合物I和线粒体DNA（mtDNA）增加，但在AMPKα2 - / -小鼠中没有增加。这可能是由于线粒体自噬减少所致，因为在运动的野生型小鼠中，含BH3结构域的BCL2家族成员BNIP3样蛋白（BNIP3L）和LC3B的表达降低，而在AMPKα2缺失的小鼠中没有这些变化。重要的是，运动增加了锰超氧化物歧化酶（MnSOD）和过氧化氢酶的表达，表明线粒体抗氧化能力增强。值得注意的是，在运动的AMPKα2 - / -小鼠中，这种抗氧化能力的提高消失了。总之，本研究表明AMPKα2通过增加动脉内皮和线粒体功能，在运动相关的血管保护中起着关键作用。
Chronic exercise training is known to protect the vasculature; however, the underlying mechanisms remain obscure. The present study hypothesized that exercise may improve aortic endothelial and mitochondrial function through an adenosine monophosphate-activated protein kinase α2 (AMPKα2)-dependent manner. Ten-week-old AMPKα2 knockout (AMPKα2−/−) mice and age-matched wild-type (WT) mice were subjected to daily treadmill running for 6 weeks, and the thoracic aorta from these mice were used for further examination. Our results showed that exercise significantly promoted vasodilatation and increased expression and phosphorylation of endothelial nitric oxide synthase (eNOS), concomitant with increased AMPKα2 expression in WT mice. These effects were not observed in AMPKα2−/− mice. Furthermore, exercise training increased thoracic aortic mitochondrial content as indicated by increased Complex I and mitochondrial DNA (mtDNA) in WT mice but not in AMPKα2−/− mice. This may be caused by decreased mitochondrial autophagy since the expression of BH3 domain-containing BCL2 family members BNIP3-like (BNIP3L) and LC3B were decreased in WT mice with exercise. And these changes were absent with AMPKα2 deletion in mice. Importantly, exercise increased the expression of manganous superoxide dismutase (MnSOD) and catalase, suggesting that mitochondrial antioxidative capacity was increased. Notably, the improved antioxidative capacity was lost in AMPKα2−/− mice with exercise. In conclusion, this study illustrated that AMPKα2 plays a critical role in exercise-related vascular protection via increasing endothelial and mitochondrial function in the artery.
登录
查看更多内容
影响因子：
21.3
作者：
通讯作者：
--
DOI：
10.1152/ajpheart.01279.2010
发表时间：
2011-10-01
影响因子：
4.8
作者：
Cacicedo, Jose M.;Gauthier, Marie-Soleil;Ido, Yasuo
通讯作者：
Ido, Yasuo
DOI：
10.1161/atvbaha.113.301717
发表时间：
2013-08-01
影响因子：
8.7
作者：
Kroeller-Schoen, Swenja;Jansen, Thomas;Schulz, Eberhard
通讯作者：
Schulz, Eberhard
影响因子：
2.8
作者：
Magnoni, Leonardo J.;Palstra, Arjan P.;Planas, Josep V.
通讯作者：
Planas, Josep V.
影响因子：
3.4
作者：
Goncalves, Ines O.;Passos, Emanuel;Magalhaes, Jose
通讯作者：
Magalhaes, Jose