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铜离子增强仙台病毒介导的细胞融合

Enhancement of Sendai virus-mediated cell fusion by cupric ions.

作者信息

Wainberg M A, Howe C, Godman G C

出版信息

J Cell Biol. 1973 May;57(2):388-96. doi: 10.1083/jcb.57.2.388.

Abstract

The effect of divalent cations on cell fusion by concentrated Sendai virus, inactivated by beta-propiolactone, was investigated using Vero and mouse L-929 cells in monolayers. With both cell lines, which are normally resistant to exogenous viral fusion, Cu(2+) in sublethal concentrations was found to promote polykaryon formation to a marked degree. The simultaneous presence of Cu(2+) and virus was required for this effect, which was thought to be related to the cytotoxic action of Cu(2+) on the cell membrane. Accordingly, under standard conditions and in the absence of virus, leakage of isotopically labeled intracellular protein was shown to bear a quantitative relationship to Cu(2+) concentration. Concomitant changes in the membrane were seen electron microscopically to consist of loss of microvilli and the appearance of numerous vesicles on, or adjacent to, the membrane. The relationship of enhanced fusibility to these toxic changes was not further elucidated. The fusion-promoting effect of Cu(2+) far exceeded that of Ca(2+); and other cations tested had no effect.

摘要

使用单层培养的非洲绿猴肾细胞(Vero细胞)和小鼠L-929细胞,研究了经β-丙内酯灭活的仙台病毒浓缩液在二价阳离子作用下的细胞融合情况。在这两种通常对外源病毒融合具有抗性的细胞系中,发现亚致死浓度的铜离子(Cu(2+))能显著促进多核体形成。这种效应需要同时存在铜离子和病毒,推测这与铜离子对细胞膜的细胞毒性作用有关。因此,在标准条件下且无病毒存在时,同位素标记的细胞内蛋白质泄漏与铜离子浓度呈定量关系。通过电子显微镜观察到,伴随的细胞膜变化包括微绒毛消失以及在细胞膜上或其附近出现大量囊泡。增强的融合能力与这些毒性变化之间的关系尚未进一步阐明。铜离子的促融合作用远超过钙离子(Ca(2+));测试的其他阳离子则无此作用。

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本文引用的文献

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