Acute exercise activates AMPK and eNOS in the mouse aorta
Acute exercise activates AMPK and eNOS in the mouse aorta
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DOI：
10.1152/ajpheart.01279.2010
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发表时间：
2011-10-01
影响因子：
4.8
通讯作者：
Ido, Yasuo
中科院分区：
文献类型：
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作者：
Cacicedo, Jose M.;Gauthier, Marie-Soleil;Ido, Yasuo
Cacicedo JM，Gauthier MS，Lebrasseur NK，Jasuja R，Ruderman NB，Ido Y.急性运动激活小鼠主动脉中的AMPK和eNOS。Am J Physiol Heart Circ Physiol 301：H1255-H1265，2011.首次发表于2011年7月1日; doi：10.1152/ajpheart.01279.2010.-运动可以防止内皮细胞（EC）功能障碍和动脉粥样硬化，即使在没有改善血脂。然而，这些影响的机制还不完全清楚。在这项研究中，我们研究了小鼠是否急性运动激活酶，可以防止EC功能障碍，如AMP激活蛋白激酶（AMPK）和内皮型一氧化氮合酶（eNOS）。我们还研究了运动是否会改变这些酶的已知调节因子。C57 BL/6小鼠进行了一次力竭性跑步机运动，之后分析了它们的肌肉中AMPK、AMPK调节蛋白、eNOS和各种酶（如AMPK）激活eNOS的情况。我们发现，这样的运动急性激活AMPK和eNOS在整个主动脉，这些影响的幅度与AMPK调节蛋白沉默信息调节因子-1（SIRT 1）-LKB 1和CaMKK β的激活和距离相关。相比之下，Akt、PKA、PKG和Src等已知激活eNOS的激酶不受影响。免疫组化显示AMPK和eNOS在主动脉内皮细胞中均被激活。这项研究提供了第一个证据表明，急性运动会激活主动脉内皮中的AMPK和eNOS。结果还表明，AMPK可能是eNOS在这种情况下的主要激活剂，其自身的激活可能由SIRT 1-LKB 1和CaMKK β介导。
Cacicedo JM, Gauthier MS, Lebrasseur NK, Jasuja R, Ruderman NB, Ido Y. Acute exercise activates AMPK and eNOS in the mouse aorta. Am J Physiol Heart Circ Physiol 301: H1255-H1265, 2011. First published July 1, 2011; doi: 10.1152/ajpheart.01279.2010.-Exercise can prevent endothelial cell (EC) dysfunction and atherosclerosis even in the absence of improvements in plasma lipids. However, the mechanisms responsible for these effects are incompletely understood. In this study we examined in mice whether an acute bout of exercise activates enzymes that could prevent EC dysfunction, such as AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS). We also examined whether exercise alters known regulators of these enzymes. C57BL/6 mice underwent a single bout of exhaustive treadmill exercise after which their aortas were analyzed for activation of AMPK, AMPK regulatory proteins, eNOS, and various enzymes that, like AMPK, activate eNOS. We found that such exercise acutely activates both AMPK and eNOS in the whole aorta and that the magnitude of these effects correlated with both the distance run and activation of the AMPK regulatory proteins silent information regulator-1 (SIRT1)-LKB1 and CaMKK beta. In contrast, Akt, PKA, PKG, and Src, other kinases known to activate eNOS, were unaffected. Immunohistochemical analysis revealed that AMPK and eNOS were both activated in the ECs of the aorta. This study provides the first evidence that an acute bout of exercise activates AMPK and eNOS in the endothelium of the aorta. The results also suggest that AMPK likely is the principal activator of eNOS in this setting and that its own activation may be mediated by both SIRT1-LKB1 and CaMKK beta.