Involvement of intracellular free Ca2+ in enhanced release of herpes simplex virus by hydrogen peroxide.

Involvement of intracellular free Ca2+ in enhanced release of herpes simplex virus by hydrogen peroxide.
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细胞内游离Ca2+参与过氧化氢释放单纯疱疹病毒。

DOI:
10.1186/1743-422x-3-62
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发表时间:
2006-08-31
期刊:
影响因子:
4.8
通讯作者:
Yura, Yoshiaki
Yura, Yoshiaki
中科院分区:
医学3区
文献类型:
--
作者:
Arimoto, Emiko;Iwai, Soichi;Sumi, Tetsuro;Ogawa, Yuzo;Yura, Yoshiaki

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据报道,通过钙离子载体升高细胞内游离Ca 2+浓度([Ca 2 +]i)增加了单纯疱疹病毒1型(HSV-1)的释放。自由扩散的过氧化氢(H2 O2)被认为可以改变Ca 2+的稳态,从而进一步增强异常的细胞活性,导致信号转导的变化和细胞功能障碍。H_2O_2对HSV-1感染细胞内[Ca ~(2+)]i的影响尚未见报道。H_2O_2处理增加了无细胞病毒的数量,降低了活细胞的比例。处理后,观察到[Ca 2 +]i升高,当细胞内和胞浆Ca 2+被Ca 2+螯合剂缓冲时,[Ca 2 +]i的升高被抑制。在Ca 2+螯合剂的存在下,H2 O2介导的无细胞病毒和细胞死亡的增加也减少。电子显微镜分析显示,在过氧化氢处理的细胞中,细胞连接处扩大,质膜局部崩解。这些结果表明,H2 O2可以升高[Ca 2 +]i,并诱导非凋亡性细胞死亡与膜损伤,这是负责增加HSV-1从上皮细胞的释放。
It was reported that elevation of the intracellular concentration of free Ca2+ ([Ca2+]i) by a calcium ionophore increased the release of herpes simplex virus type 1 (HSV-1). Freely diffusible hydrogen peroxide (H2O2) is implied to alter Ca2+ homeostasis, which further enhances abnormal cellular activity, causing changes in signal transduction, and cellular dysfunction. Whether H2O2 could affect [Ca2+]i in HSV-1-infected cells had not been investigated. H2O2 treatment increased the amount of cell-free virus and decreased the proportion of viable cells. After the treatment, an elevation in [Ca2+]i was observed and the increase in [Ca2+]i was suppressed when intracellular and cytosolic Ca2+ were buffered by Ca2+ chelators. In the presence of Ca2+ chelators, H2O2-mediated increases of cell-free virus and cell death were also diminished. Electron microscopic analysis revealed enlarged cell junctions and a focal disintegration of the plasma membrane in H2O2-treated cells. These results indicate that H2O2 can elevate [Ca2+]i and induces non-apoptotic cell death with membrane lesions, which is responsible for the increased release of HSV-1 from epithelial cells.