Exercise training induces a cardioprotective phenotype and alterations in cardiac subsarcolemmal and intermyofibrillar mitochondrial proteins
Exercise training induces a cardioprotective phenotype and alterations in cardiac subsarcolemmal and intermyofibrillar mitochondrial proteins
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DOI：
10.1152/ajpheart.01278.2008
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发表时间：
2009-07-01
影响因子：
4.8
通讯作者：
Powers, Scott K.
中科院分区：
文献类型：
--
作者：
Kavazis, Andreas N.;Alvarez, Sophie;Powers, Scott K.
卡瓦赞，阿尔瓦雷斯·S，塔尔伯特·E，李·Y，鲍尔斯·SK。运动训练诱导心脏保护表型和心肌肌膜下和肌原纤维间线粒体蛋白的改变。Am J Physiol心圈Physiol 297：H144-H152,2009。2008年5月8日首次出版；DOI：10.1152/ajpheart.01278.2008。-耐力运动被认为对缺血再灌注引起的心肌损伤提供心脏保护，线粒体适应可能在这种保护中发挥关键作用。为了研究运动诱导的线粒体蛋白的变化，我们比较了从安静(对照)和运动训练的SpragueDawley大鼠的心肌中分离的肌膜下和肌原纤维间线粒体的蛋白质组。为了实现这一目标，我们利用等压标签进行相对和绝对定量，这使得可以在多个样本之间同时识别和定量蛋白质。该方法共鉴定出222种心肌线粒体蛋白。重要的是，与久坐不动的对照组动物相比，反复的耐力运动导致肌原纤维间线粒体内11种蛋白质发生显著变化(7种增加，4种减少)。此外，运动训练导致肌膜下线粒体中两种蛋白质的显著变化(一种增加，一种减少)，与久坐的对照组动物相比。差异表达的蛋白质可以分为七个功能基团，并鉴定了几个新的和潜在重要的心脏保护介质。我们的结论是，耐力运动导致线粒体蛋白质组的改变，这可能有助于心脏保护表型。重要的是，根据我们的发现，可以使用药物或其他干预措施来开发一种在缺血发作期间保护心肌的策略。
Kavazis AN, Alvarez S, Talbert E, Lee Y, Powers SK. Exercise training induces a cardioprotective phenotype and alterations in cardiac subsarcolemmal and intermyofibrillar mitochondrial proteins. Am J Physiol Heart Circ Physiol 297: H144-H152, 2009. First published May 8, 2008; doi:10.1152/ajpheart.01278.2008.-Endurance exercise is known to provide cardioprotection against ischemia-reperfusion-induced myocardial injury, and mitochondrial adaptations may play a critical role in this protection. To investigate exercise-induced changes in mitochondrial proteins, we compared the proteome of subsarcolemmal and intermyofibrillar mitochondria isolated from the myocardium of sedentary (control) and exercise-trained Sprague-Dawley rats. To achieve this goal, we utilized isobaric tags for relative and absolute quantitation, which allows simultaneous identification and quantification of proteins between multiple samples. This approach identified a total of 222 cardiac mitochondrial proteins. Importantly, repeated bouts of endurance exercise resulted in significant alterations in 11 proteins within intermyofibrillar mitochondria (seven increased; four decreased) compared with sedentary control animals. Furthermore, exercise training resulted in significant changes in two proteins within subsarcolemmal mitochondria (one increased; one decreased) compared with sedentary control animals. Differentially expressed proteins could be classified into seven functional groups, and several novel and potentially important cardioprotective mediators were identified. We conclude that endurance exercise induces alterations in mitochondrial proteome that may contribute to cardioprotective phenotype. Importantly, based on our findings, pharmacological or other interventions could be used to develop a strategy of protecting the myocardium during an ischemic attack.