Cardiac, skeletal, and smooth muscle mitochondrial respiration: are all mitochondria created equal?
Cardiac, skeletal, and smooth muscle mitochondrial respiration: are all mitochondria created equal?
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DOI：
10.1152/ajpheart.00227.2014
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发表时间：
2014-08-01
影响因子：
4.8
通讯作者：
Richardson, Russell S.
中科院分区：
文献类型：
--
作者：
Park, Song-Young;Gifford, Jayson R.;Richardson, Russell S.
与心肌和骨骼肌不同，对血管平滑肌线粒体呼吸知之甚少。因此，本研究检测了健康人供血动脉平滑肌中的线粒体呼吸速率，并与健康心脏和骨骼肌的线粒体呼吸速率进行了比较。从总共22名受试者（53 +/- 6岁）中采集心脏、骨骼肌和平滑肌，并在透化纤维中评估线粒体呼吸。复合体I + II，状态3呼吸，氧化磷酸化能力的指标，从心肌到骨骼肌再到平滑肌逐渐下降（分别为54 +/- 1，39 +/- 4和15 +/- 1 pmol.s（-1）.mg（-1），P < 0.05）。柠檬酸合酶（CS）活性是线粒体密度的一个指数，从心肌到骨骼肌再到平滑肌也逐渐下降（分别为222 +/- 13、115 +/- 2和48 +/- 2 μ mol.g（-1）.min（-1），P < 0.05）。因此，当呼吸速率由CS（呼吸/线粒体含量）标准化时，氧化磷酸化能力在三种肌肉类型之间不再不同。有趣的是，对于CS活性标准化的复合物I状态2（每线粒体含量的非磷酸化呼吸的指数）从心肌到骨骼肌到平滑肌逐渐增加，使得呼吸控制比率（状态3/状态2呼吸）从心肌到骨骼肌到平滑肌逐渐下降（分别为5.3 +/- 0.7、3.2 +/- 0.4和1.6 +/- 0.3 pmol.s（-1）.mg（-1），P < 0.05）。因此，虽然氧化磷酸化能力每线粒体内容在心脏，骨骼肌和平滑肌表明所有的线粒体是平等的，对比呼吸控制率和非磷酸化呼吸突出这些肌肉线粒体之间的内在功能差异的存在。这可能会影响氧化磷酸化的效率，并可能改变ROS的产生。
Unlike cardiac and skeletal muscle, little is known about vascular smooth muscle mitochondrial respiration. Therefore, the present study examined mitochondrial respiratory rates in smooth muscle of healthy human feed arteries and compared with that of healthy cardiac and skeletal muscles. Cardiac, skeletal, and smooth muscles were harvested from a total of 22 subjects (53 +/- 6 yr), and mitochondrial respiration was assessed in permeabilized fibers. Complex I + II, state 3 respiration, an index of oxidative phosphorylation capacity, fell progressively from cardiac to skeletal to smooth muscles (54 +/- 1, 39 +/- 4, and 15 +/- 1 pmol.s(-1).mg(-1), P < 0.05, respectively). Citrate synthase (CS) activity, an index of mitochondrial density, also fell progressively from cardiac to skeletal to smooth muscles (222 +/- 13, 115 +/- 2, and 48 +/- 2 mu mol.g(-1).min(-1), P < 0.05, respectively). Thus, when respiration rates were normalized by CS (respiration per mitochondrial content), oxidative phosphorylation capacity was no longer different between the three muscle types. Interestingly, complex I state 2 normalized for CS activity, an index of nonphosphorylating respiration per mitochondrial content, increased progressively from cardiac to skeletal to smooth muscles, such that the respiratory control ratio, state 3/state 2 respiration, fell progressively from cardiac to skeletal to smooth muscles (5.3 +/- 0.7, 3.2 +/- 0.4, and 1.6 +/- 0.3 pmol.s(-1).mg(-1), P < 0.05, respectively). Thus, although oxidative phosphorylation capacity per mitochondrial content in cardiac, skeletal, and smooth muscles suggest all mitochondria are created equal, the contrasting respiratory control ratio and nonphosphorylating respiration highlight the existence of intrinsic functional differences between these muscle mitochondria. This likely influences the efficiency of oxidative phosphorylation and could potentially alter ROS production.