Porcine circovirus type 2 capsid protein induces unfolded protein response with subsequent activation of apoptosis

作     者：Ying-shan ZHOU Yuan-xing GU Bao-zhu QI Yi-kai ZHANG Xiao-liang LI Wei-huan FANG 

作者机构：College of Animal Science and TechnologyZhejiang Provincial Engineering Laboratory for Animal Health Inspection & Internet TechnologyZhejiang A&F University Institute of Preventive Veterinary MedicineZhejiang University 

出 版 物：《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 (浙江大学学报（英文版）B辑（生物医学与生物技术）)

年 卷 期：2017年第18卷第4期

页      面：316-323页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 090601[农学-基础兽医学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1001[医学-基础医学(可授医学、理学学位)] 0905[农学-畜牧学] 0906[农学-兽医学] 09[农学] 

基　　金：supported by the National Natural Science Foundation of China(No.31272534) the Department of Education of Zhejiang Province(No.Y201635576),China 

主　　题：Porcine circovirus 2 Capsid protein Unfolded protein response Apoptosis 

摘      要：Porcine circovirus type 2（PCV2）has recently been reported to elicit the unfolded protein response（UPR）via activation of the PERK/e IF2α（RNA-activated protein kinase-like endoplasmic reticulum（ER）kinase/eukaryotic initiation factor 2α）*** study attempted to examine which viral protein might be involved in inducing UPR and whether this cellular event would lead to apoptosis of the cells expressing the viral *** transient expression,we found that both replicase（Rep）and capsid（Cap）proteins of PCV2 could induce ER stress as shown by increased phosphorylation of PERK with subsequent activation of the eI F2α-ATF4（activating transcription factor 4）-CHOP（CCAAT/enhancer-binding protein homologous protein）*** expression,but not Rep,significantly reduced antiapoptotic B-cell lymphoma-2（Bcl-2）and increased caspase-3 cleavage,possibly due to increased expression of *** knockdown of PERK by RNA interference clearly reduced Cap-induced CHOP expression,caspase-3cleavage,and apoptotic cell death possibly by partially rescuing Bcl-2 expression,we propose that there is connection between Cap-induced UPR and apoptosis via the PERK/eI F2α/ATF4/CHOP/Bcl-2 *** study,together with our earlier studies,provides insight into the mechanisms underlying PCV2 pathogenesis.