Varicella-zoster virus-induced apoptosis in MeWo cells is accompanied by down-regulation of Bcl-2 expression.
Varicella-zoster virus-induced apoptosis in MeWo cells is accompanied by down-regulation of Bcl-2 expression.
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DOI：
10.3109/13550281003682547
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发表时间：
2010-03
影响因子：
3.2
通讯作者：
Pugazhenthi S
中科院分区：
文献类型：
--
作者：
Brazeau E;Mahalingam R;Gilden D;Wellish M;Kaufer BB;Osterrieder N;Pugazhenthi S
水痘-带状疱疹病毒感染培养中的多个人和猴子细胞。细胞死亡的方式似乎是自噬或凋亡。对VZV感染的人黑色素瘤细胞的分析表明，Bcl2mRNA和蛋白水平在感染后72hPI和显著降低，并伴随着细胞色素c从线粒体释放到细胞质中。对感染病毒的细胞进行Western印迹分析发现，在和72HPI处，caspase-8和caspase-9激活，caspase-8和caspase-9分别是外在途径的标志和内在途径的标志。裂解caspase-3和裂解多聚(ADP)核糖聚合酶(PARP)的水平也在细胞病变效应的高峰期显著增加。因此，VZV可诱导MeWo细胞发生凋亡，其中Bcl2表达下调。未来的研究将确定与允许VZV潜伏的神经元相比，非神经元细胞中的级联凋亡事件的差异。
Varicella-zoster virus infects multiple human and monkey cells in culture. The mode of cell death appears to be autophagy or apoptosis. Analysis of VZV-infected human melanoma (MeWo) cells revealed that Bcl-2 mRNA and protein levels were decreased significantly 64 and 72 hpi (hours post infection), accompanied by the release of cytochrome c from mitochondria into the cytoplasm. Western blot analysis of virus-infected cells revealed activation of caspase-8, a marker for the extrinsic pathway of apoptosis, and caspase-9, a marker for the intrinsic pathway of apoptosis at 64 and 72 hpi. Significant increases in the levels of cleaved caspase-3 and cleaved poly (ADP) ribose polymerase (PARP) were also seen at the height of cytopathic effect. Thus VZV induces apoptosis in MeWo cells in which Bcl-2 is down-regulated. Future studies will determine differences in the cascade of apoptotic events in non-neuronal cells compared to neurons that allow VZV to become latent.
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影响因子：
5.4
作者：
Tischer, B. Karsten;Kaufer, Benedikt B.;Osterrieder, Nikolaus
通讯作者：
Osterrieder, Nikolaus
影响因子：
3.8
作者：
SADZOTDELVAUX, C;THONARD, P;REUTIER, B
通讯作者：
REUTIER, B
影响因子：
5.4
作者：
Hood, C;Cunningham, AL;Abendroth, A
通讯作者：
Abendroth, A
影响因子：
5.8
作者：
König, A;Hömme, C;Wolff, MH
通讯作者：
Wolff, MH
影响因子：
5.4
作者：
Pugazhenthi, Subbiah;Gilden, Donald H.;Mahalingam, Ravi
通讯作者：
Mahalingam, Ravi