McCarthy J V, Cotter T G
Department of Biochemistry, University College Cork, Lee Maltings, Prospect Row, Cork, Ireland.
Cell Death Differ. 1997 Dec;4(8):756-70. doi: 10.1038/sj.cdd.4400296.
In this study we have shown that redistribution of the lipid composition of the external and internal leaflets of the PM during apoptosis results in two main alterations in the cell surface, externalisation of PS, and a looser packing of the lipid hydrophobic head groups in the external leaflet. Significantly, neither of these alterations can be directly implicated in the mechanism of apoptotic cell shrinkage, however they do have functions in other phases of the apoptotic process. Progressional studies involving morphological and flow cytometric evaluation, and DNA gel electrophoresis revealed that apoptotic cell shrinkage is associated with a decrease in [Na+]i and [K+]i which occurs after visualisation of chromatin condensation and internucleosomal DNA fragmentation, and prior to apoptotic body formation. When apoptotic cultures were supplemented with inhibitors of the Na+, K+-ATPase pump or the Ca2+-dependent K+ channel, essentially all of the respective Na+ or K+ efflux during apoptosis can be inhibited, suggesting that essentially all of the Na+ and K+ efflux can be ascribed to active pumping via the Na+, K+-ATPase pump and the Ca2+-dependent K+ channel.
在本研究中,我们已经表明,细胞凋亡过程中质膜(PM)外小叶和内小叶脂质组成的重新分布导致细胞表面出现两个主要变化,即磷脂酰丝氨酸(PS)外化,以及外小叶中脂质疏水头部基团排列更松散。值得注意的是,这些变化均不能直接归因于凋亡细胞皱缩的机制,然而它们在凋亡过程的其他阶段确实具有功能。涉及形态学和流式细胞术评估以及DNA凝胶电泳的进一步研究表明,凋亡细胞皱缩与细胞内[Na⁺]和[K⁺]的减少有关,这种减少发生在染色质凝聚和核小体间DNA片段化出现之后、凋亡小体形成之前。当向凋亡细胞培养物中添加Na⁺,K⁺-ATP酶泵或Ca²⁺依赖性K⁺通道的抑制剂时,凋亡过程中基本上所有相应的Na⁺或K⁺外流都可以被抑制,这表明基本上所有的Na⁺和K⁺外流都可归因于通过Na⁺,K⁺-ATP酶泵和Ca²⁺依赖性K⁺通道的主动转运。