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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Serum deprivation increases ceramide levels and induces apoptosis in undifferentiated HN9.10e cells.
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Serum deprivation increases ceramide levels and induces apoptosis in undifferentiated HN9.10e cells.

机译：血清剥夺增加未分化的HN9.10e细胞中的神经酰胺水平并诱导凋亡。

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摘要

Sphingolipid metabolites have been involved in the regulation of proliferation, differentiation and apoptosis. While cellular mechanisms of these processes have been extensively analysed in the post-mitotic neurons, little is known about proliferating neuronal precursors. We have taken as a model of neuroblasts the embryonic hippocampal cell line HN9.10e. Apoptosis was induced by serum deprivation and by treatment with N-acetylsphingosine (C2-Cer), a membrane-permeant analogue of the second messenger ceramide. Following C2-Cer addition, cytochrome c was released from mitochondria, [Ca(2+)](i) and caspase-3-like activity increased. Both cytochrome c release and rise of [Ca(2+)](i) occurred before caspase-3 activation and nuclear condensation. The intracellular levels of ceramide peaked at 1h following the serum deprivation. These results indicate that the serum deprivation induces a rise in the intracellular ceramide level, and that increased ceramide concentration leads to calcium dysregulation and release of cytochrome c followed by caspase-3 activation. We show that cytochrome c is released without a loss of mitochondrial transmembrane potential.
机译：鞘脂代谢物已经参与了增殖，分化和凋亡的调节。尽管在有丝分裂后的神经元中已广泛分析了这些过程的细胞机制，但对增殖神经元前体知之甚少。我们已将胚胎海马细胞系HN9.10e用作神经母细胞的模型。通过血清剥夺和用N-乙酰基鞘氨醇（C2-Cer）（第二种信使神经酰胺的膜渗透性类似物）治疗诱导细胞凋亡。添加C2-Cer后，细胞色素c从线粒体中释放出来，[Ca（2 +）]（i）和caspase-3-like活性增加。细胞色素c的释放和[Ca（2 +）]（i）的上升都发生在caspase-3激活和核浓缩之前。血清剥夺后1小时，神经酰胺的细胞内水平达到峰值。这些结果表明，血清剥夺引起细胞内神经酰胺水平的升高，并且神经酰胺浓度的升高导致钙失调和细胞色素c的释放，随后激活caspase-3。我们显示出细胞色素c被释放而没有线粒体跨膜潜力的损失。

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