Pseudorabies virus infection induces endoplasmic reticulum stress and unfolded protein response in suspension-cultured BHK-21 cells
文献类型： 外文期刊
作者： Chen, Li 1 ; Ni, Minshu 2 ; Ahmed, Waqas 1 ; Xu, Yue 2 ; Bao, Xi 2 ; Zhuang, Tenghan 2 ; Feng, Lei 2 ; Guo, Meijin 1 ;
作者机构： 1.East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China
2.Jiangsu Acad Agr Sci, Inst Vet Immunol & Engn, Natl Res Ctr Engn & Technol Vet Biol, Nanjing, Jiangsu, Peoples R China
3.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou, Jiangsu, Peoples R China
4.Jiangsu Univ, Sch Pharm, Zhenjiang, Jiangsu, Peoples R China
关键词： BHK-21 cells; endoplasmic reticulum stress; Pseudorabies virus; unfolded protein response
期刊名称：JOURNAL OF GENERAL VIROLOGY （ 影响因子：3.8； 五年影响因子：3.8 ）
ISSN： 0022-1317
年卷期： 2022 年 103 卷 12 期
页码：
收录情况： SCI
摘要： Viral infections cause endoplasmic reticulum (ER) stress and subsequently unfolded protein response (UPR) which restores ER homeostasis. In this study, levels of proteins or transcription of three UPR pathways were examined in suspension-cultured BHK-21 cells to investigate Pseudorabies virus (PRV) infection-induced ER stress, in which glucose-related proteins 78 kD and 94 kD (GRP78 and GRP94) were upregulated. The downstream double-stranded RNA-activated protein kinase-like ER kinase (PERK) pathway was activated with upregulation of ATF4, CHOP, and GADD34, and the inositol requiring kinase 1 (IRE1) pathway was triggered by the splicing of X box-binding protein 1 (XBP1) mRNA and the enhanced expression of p58IPK and EDEM. Furthermore, our results showed that the ER stress, induced by 0.005 mu M thapsigargin, promoted PRV replication in suspension-cultured BHK-21 cells, and that PRV glycoprotein B (gB) overexpression triggered the PERK and IRE1 pathways.
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