Position: Home > Articles > P58IPK Regulates Porcine Circovirus Type 2-induced Autophagy through PERK/eIF2α Pathway
Chinese Journal of Animal and Veterinary Sciences
2017
(11)
2125-2134
P58IPK通过PERK/eIF2α通路调控猪圆环病毒2型所诱导的细胞自噬
作 者：
杨了寒;王凯;许苏童;张敏;胡林;何启盖;张淑君
关键词：
P58IPK;内质网应激;细胞自噬;PERK;PCV2;ATG12
摘 要：
旨在研究猪圆环病毒2型(PCV2)感染激活的PERK/eIF2α通路是否与细胞自噬相关,以及过表达分子伴侣蛋白P58IPK在其中的作用。首先通过PERK特异性抑制剂GSK2606414和siRNA及蛋白免疫印迹检测磷酸化eIF2α(p-eIF2α)、LC3-Ⅱ和ATG5-ATG12蛋白表达,研究PCV2感染PK-15细胞24h后PERK/eIF2α通路与细胞自噬的关系;然后通过构建和瞬时转染P58IPK真核过表达质粒及蛋白免疫印迹研究过表达P58IPK对PCV2感染PK-15诱导的PERK/eIF2α通路及细胞自噬的影响。结果显示,PERK特异性抑制剂GSK2606414和siRNA干扰PERK可极显著抑制PCV2诱导的p-eIF2α(P<0.01)和LC3-Ⅱ(P<0.01)表达;而过表达P58IPK同样可以极显著下调PCV2诱导的p-eIF2α(P<0.01)、ATG5-ATG12(P<0.01)及LC3-Ⅱ(P<0.01),且能极显著下调PCV2拷贝数(P<0.01)。结果表明,PCV2感染PK-15通过激活PERK/eIF2α通路诱导细胞自噬,过表达P58IPK通过抑制PERK通路抑制PCV2诱导的细胞自噬,从而抑制病毒复制。
译 名：
P58IPK Regulates Porcine Circovirus Type 2-induced Autophagy through PERK/eIF2α Pathway
作 者：
YANG Liao-han;WANG Kai;XU Su-tong;ZHANG Min;HU Lin;HE Qi-gai;ZHANG Shu-jun;Key Laboratory of Agricultural Animal Genetics,Breeding and Reproduction of Ministry of Education,College of Animal Science and Technology,Huazhong Agricultural University;The State Key Laboratory of Agricultural Microbiology,Huazhong Agricultural University;
单 位：
Key Laboratory of Agricultural Animal Genetics,Breeding and Reproduction of Ministry of Education,College of Animal Science and Technology,Huazhong Agricultural University%The State Key Laboratory of Agricultural Microbiology,Huazhong Agricultural University
关键词：
P58IPK;;ER stress;;autophagy;;PERK;;PCV2;;ATG12
摘 要：
This experiment was conducted to study the relationship between porcine circovirus type2(PCV2)infection activated PERK/eIF2αpathway and autophagy,and the possible function of overexpressing chaperone P58 IPK within it.PK-15 cells were treated with PERK specific inhibitor GSK2606414,siRNA,followed by PCV2 infection for 24 h.Western blot was taken to measure phosphorylated eIF2α(p-eIF2α),LC3-Ⅱ and ATG5-ATG12 expression at first.Then P58 IPK overexpression vector was constructed and transiently transfected,combined with Western blot to study the influence of overexpressing P58 IPK on PCV2-induced PERK/eIF2αpathway and autophagy.Western blot results showed PERK specific inhibitor GSK2606414 and siRNAsignificantly suppressed PCV2-induced p-eIF2α(P<0.01)and LC3-Ⅱ(P<0.01)expression.While overexpressing P58 IPK not only resulted in PCV2-induced p-eIF2α(P<0.01),ATG5-ATG12(P<0.01)and LC3-Ⅱ(P<0.01)decrease,but also significantly downregulated activating PCV2 copies number(P<0.01).Results indicate PCV2 infection induces autophagy through activating PERK/eIF2αpathway.Overexpression of P58 IPK represses PCV2-induced autophagy through inhibiting PERK pathway,consequently,inhibiting PCV2 replication.
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