Evidence of a novel event during neuronal death: Development of competence-to-die in response to cytoplasmic cytochrome c
Evidence of a novel event during neuronal death: Development of competence-to-die in response to cytoplasmic cytochrome c
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DOI：
10.1016/s0896-6273(00)80587-5
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发表时间：
1998-10-01
期刊：
影响因子：
16.2
通讯作者：
Johnson, EM
中科院分区：
文献类型：
--
作者：
Deshmukh, M;Johnson, EM
神经生长因子（NGF）剥夺后发生程序性细胞死亡的交感神经元显示出线粒体中细胞色素c的蛋白质合成依赖性和bax依赖性损失。然而，细胞质显微注射细胞色素c不足以诱导维持ngf的交感神经元细胞死亡。相比之下，细胞色素c微注射可迅速诱导缺乏ngf、bax缺乏或缺乏ngf、环己亚胺处理的神经元发生caspase依赖性死亡。细胞需要被剥夺NGF 15-20小时，才能通过注射细胞色素c获得死亡能力。这些数据表明，NGF剥夺诱导了细胞色素c的易位和另一个事件，我们称之为能力死亡，这是独立于大分子合成和BAX功能的。这两个过程都是神经元发生凋亡所必需的。
Sympathetic neurons undergoing programmed cell death after nerve growth factor (NGF) deprivation are shown to exhibit a protein synthesis-dependent, BAX-dependent loss of cytochrome c from the mitochondria. However, cytoplasmic microinjection of cytochrome c was insufficient to induce cell death in NGF-maintained sympathetic neurons. In contrast, microinjection of cytochrome c rapidly induced a caspase-dependent death in NGF-deprived, Bax-deficient or NGF-deprived, cycloheximide-treated neurons. Cells needed to be deprived of NGF for 15-20 hr before they acquired competence to die with injection of cytochrome c. These data suggest that NGF deprivation induced the translocation of cytochrome c and another event, which we term as competence-to-die, that was independent of macromolecular synthesis and BAX function. Both these processes were required for neurons to undergo apoptosis.