Phosphorylation of p38 MAPK and its downstream targets in SARS coronavirus-infected cells.
Phosphorylation of p38 MAPK and its downstream targets in SARS coronavirus-infected cells.
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DOI：
10.1016/j.bbrc.2004.05.107
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发表时间：
2004-07-09
影响因子：
3.1
通讯作者：
Morikawa S
中科院分区：
文献类型：
--
作者：
Mizutani T;Fukushi S;Saijo M;Kurane I;Morikawa S
严重急性呼吸系统综合症（SARS）已成为全球突发公共卫生事件。了解SARS诱导的细胞病变效应（cpe）的分子机制是预防SARS的合理途径，而了解病毒感染诱导的细胞应激反应对理解cpe具有重要意义。识别核衣壳(N)和膜(M)蛋白的多克隆抗体在感染后至少6和12 h分别检测到病毒感染的Vero E6细胞中的病毒N和M蛋白。此外，在24hpi时检测病毒感染细胞的DNA阶梯和裂解caspase-3，表明SARS-CoV感染诱导细胞凋亡。在sars - cov感染的细胞中，p38 MAPK的磷酸化在18 hp时显著上调。p38 MAPK、MAPKAPK-2、HSP-27、CREB和eIF4E的下游靶标在病毒感染的细胞中磷酸化。p38 MAPK抑制剂SB203580可有效抑制sars - cov感染细胞中HSP-27、CREB和eIF4E的磷酸化。然而，SB203580处理不影响病毒蛋白的合成。
Severe acute respiratory syndrome (SARS) has become a global public health emergency. Understanding the molecular mechanisms of SARS-induced cytopathic effects (CPEs) is a rational approach for the prevention of SARS, and an understanding of the cellular stress responses induced by viral infection is important for understanding the CPEs. Polyclonal antibodies, which recognized nucleocapsid (N) and membrane (M) proteins, detected viral N and M proteins in virus-infected Vero E6 cells at least 6 and 12 h post-infection (h.p.i.), respectively. Furthermore, detection of DNA ladder and cleaved caspase-3 in the virus-infected cells at 24 h.p.i. indicated that SARS-CoV infection induced apoptotic cell death. Phosphorylation of p38 MAPK was significantly up-regulated at 18 h.p.i. in SARS-CoV-infected cells. The downstream targets of p38 MAPK, MAPKAPK-2, HSP-27, CREB, and eIF4E were phosphorylated in virus-infected cells. The p38 MAPK inhibitor, SB203580, inhibited effectively phosphorylation of HSP-27, CREB, and eIF4E in SARS-CoV-infected cells. However, viral protein synthesis was not affected by treatment of SB203580.
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