The cell-rounding activity of the vesicular stomatitis virus matrix protein is due to the induction of cell death
The cell-rounding activity of the vesicular stomatitis virus matrix protein is due to the induction of cell death
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DOI：
10.1128/jvi.77.9.5524-5528.2003
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发表时间：
2003-05-01
影响因子：
5.4
通讯作者：
Lyles, DS
中科院分区：
文献类型：
--
作者：
Kopecky, SA;Lyles, DS
在没有其他病毒成分的情况下表达的水疱性口炎病毒 (VSV) 的基质 (M) 蛋白会引起 VSV 的许多细胞病变效应，包括抑制宿主基因表达和诱导细胞变圆。最近的研究表明，在没有其他病毒成分的情况下，M 蛋白也能诱导细胞凋亡。这提出了细胞凋亡途径的激活导致M蛋白抑制宿主基因表达和细胞变圆的可能性。为了检验这一假设，将 M mRNA 转染到稳定过表达 Bcl-2 的 HeLa 细胞（HeLa-Bcl-2 细胞）后，对宿主基因表达和细胞圆化进行了分析。我们之前已经证明 Bcl-2 抑制 M 蛋白诱导的细胞凋亡。在这里，我们表明 M 蛋白抑制宿主基因表达不需要激活 Bcl-2 下游的凋亡途径。相反，Bcl-2的过表达抑制M蛋白诱导的细胞圆整，表明Bcl-2下游的凋亡途径是M蛋白的细胞圆整活性所必需的。
The matrix (M) protein of vesicular stomatitis virus (VSV) expressed in the absence of other viral components causes many of the cytopathic effects of VSV, including an inhibition of host gene expression and the induction of cell rounding. It was recently shown that M protein also induces apoptosis in the absence of other viral components. This raises the possibility that the activation of apoptotic pathways causes the inhibition of host gene expression and cell rounding by M protein. To test this hypothesis, host gene expression and cell rounding were analyzed after the transfection of M mRNA into HeLa cells stably overexpressing Bcl-2 (HeLa-Bcl-2 cells). We have shown previously that Bcl-2 inhibits M-protein-induced apoptosis. Here, we show that activation of the apoptotic pathways downstream of Bcl-2 is not required for the inhibition of host gene expression by M protein. In contrast, overexpression of Bcl-2 inhibited cell rounding induced by M protein, indicating that apoptotic pathways downstream of Bcl-2 are required for the cell-rounding activities of M protein.