Coxsackievirus A16 infection triggers apoptosis in RD cells by inducing ER stress.
Coxsackievirus A16 infection triggers apoptosis in RD cells by inducing ER stress.
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DOI：
10.1016/j.bbrc.2013.10.142
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发表时间：
2013-11
影响因子：
3.1
通讯作者：
Guo-guo Zhu;Yingcheng Zheng;lianglu zhang;Yingying Shi;Wenhua Li;Zhongchun Liu;B. Peng;Jun Yin;Wanhong Liu;Xiaohua He
中科院分区：
文献类型：
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作者：
Guo-guo Zhu;Yingcheng Zheng;lianglu zhang;Yingying Shi;Wenhua Li;Zhongchun Liu;B. Peng;Jun Yin;Wanhong Liu;Xiaohua He
由于病毒的流行，导致手足口病(HFMD)的柯萨奇病毒A16(CA16)感染已成为亚洲常见的健康问题。因此，了解CA16感染的发病机制具有重要意义。诱导内质网(ER)应激的病毒面临未折叠蛋白应答(UPR)，UPR可能导致细胞凋亡并影响病毒复制。在本研究中，我们发现CA16感染可以诱导RD细胞的凋亡和内质网应激。有趣的是，通过激活内源性或外源性caspase-3、-8和-9，RD细胞的凋亡被4-苯基丁酸(4PBA)抑制，4-苯基丁酸(4PBA)是一种减轻内质网应激的化学伴侣。这些结果表明，CA16感染导致内质网应激，进而导致内质网应激诱导的细胞凋亡延长。本研究为了解CA16感染和宿主反应提供了新的基础。
Coxsackievirus A16 (CA16) infection, which is responsible for hand, foot and mouth disease (HFMD), has become a common health problem in Asia due to the prevalence of the virus. Thus, it is important to understand the pathogenesis of CA16 infection. Viruses that induce endoplasmic reticulum (ER) stress are confronted with the unfolded protein response (UPR), which may lead to apoptotic cell death and influence viral replication. In this study, we found that CA16 infection could induce apoptosis and ER stress in RD cells. Interestingly, apoptosis via the activation of caspase-3, -8 and -9 in the extrinsic or intrinsic apoptotic pathways in RD cells was inhibited by 4-phenyl butyric acid (4PBA), a chemical chaperone that reduces ER stress. These results suggest that CA16 infection leads to ER stress, which in turn results in prolonged ER stress-induced apoptosis. This study provides a new basis for understanding CA16 infection and host responses.