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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Outer mitochondrial membrane permeability can regulate coupled respiration and cell survival
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Outer mitochondrial membrane permeability can regulate coupled respiration and cell survival

机译：线粒体外膜通透性可调节呼吸和细胞存活率

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摘要

Coupled cellular respiration requires that ATP and ADP be effi- ciently exchanged between the cytosol and the mitochondrial matrix. When growth factors are withdrawn from dependent cells, metabolism is disrupted by a defect in ATP/ADP exchange across the mitochondrial membranes. Unexpectedly. we find that this defect results from loss of outer mitochondrial membrane perme- ability to metabolic anions. This decrease in anion permeability correlates with the changes in conductance properties that accom- pany closure of the voltage-dependent anion channel (also known as mitochondrial porin). Loss of outer membrane permeability (Ⅰ) results in the accumulation of stored metabolic energy within the intermembrane space in the form of creatine phosphate, (Ⅱ) is prevented by the outer mitochondrial membrane proteins Bcl-x_L and Bcl-2, and (Ⅲ) can be reversed by growth factor readdition. If outer membrane impermeability persists, the disruption of mito- chondrial homeostasis culminates in loss of outer mitochondrial membrane integrity, cytochrome c redistribution, and apoptosis. The recognition that outer membrane permeability is regulated under physiological conditions has important implications for the understanding of bioenergetics and cell survival.
机译：耦合的细胞呼吸作用要求在细胞质和线粒体基质之间有效地交换ATP和ADP。当从依赖细胞中撤出生长因子时，新陈代谢会被跨线粒体膜的ATP / ADP交换缺陷所破坏。不料。我们发现，这种缺陷是由于线粒体外膜通透性对新陈代谢阴离子的损失所致。阴离子渗透率的下降与电导特性的变化相关，电导特性的变化伴随着电压依赖性阴离子通道（也称为线粒体孔蛋白）的闭合。外膜通透性的丧失（Ⅰ）导致肌内磷酸酶形式的膜间空间内储存的代谢能量的积累，（Ⅱ）被线粒体外膜蛋白Bcl-x_L和Bcl-2阻止，以及（Ⅲ）可以通过生长因子的逆转逆转。如果外膜的不渗透性持续存在，那么线粒体稳态的破坏将最终导致线粒体外膜完整性的丧失，细胞色素c的重新分布和细胞凋亡。外膜通透性在生理条件下调节的认识对于理解生物能学和细胞存活具有重要意义。

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