程序性细胞死亡因子10抑制Ⅰ型干扰素表达并促进FMDV复制  

Programmed Cell Death Factor 10 Inhibits TypeⅠInterferon Expression and Promotes the Replication of Foot-and-mouth Disease Virus

作　　者：曾宗波 马旭升 罗志宽 齐亚银[1] 郑海学[2] ZENG Zongbo;MA Xusheng;LUO Zhikuan;QI Yayin;ZHENG Haixue(College of Animal Science and Technology, Shihezi University, Shihezi832000, China;State Key Laboratory of Veterinary Etiological Biology, National Foot-and-Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China)

机构地区：[1]石河子大学动物科技学院,石河子832000 [2]中国农业科学院兰州兽医研究所,家畜疫病病原学国家重点实验室,兰州730046

出　　处：《畜牧兽医学报》2021年第2期450-459,共10页ACTA VETERINARIA ET ZOOTECHNICA SINICA

基　　金：国家自然科学基金(31760737)。

摘　　要：旨在探究宿主蛋白程序性细胞死亡因子10(programmed cell death factor 10,PDCD10)通过抑制Ⅰ型干扰素表达进而促进口蹄疫病毒(foot-and-mouth disease virus,FMDV)的复制。首先,本研究验证了过表达和沉默PDCD10对FMDV复制的影响,接着利用双荧光素酶报告系统探究PDCD10对Ⅰ型干扰素信号通路活化的影响,最后,利用实时荧光定量PCR探究PDCD10对Ⅰ型干扰素通路下游刺激基因(IFN-stimulated genes,ISGs)转录的影响。结果表明,过表达PDCD10显著促进FMDV的复制,沉默PDCD10显著抑制FMDV的复制。与对照相比,过表达PDCD10后感染仙台病毒(Sendai virus,SeV)的细胞培养液上清液显著促进FMDV复制,进一步,PDCD10显著抑制SeV诱导的IFN-β启动子以及NF-κB的激活且呈剂量依赖性,并且PDCD10负调控Ⅰ型干扰素通路信号分子转录,最后还发现PDCD10负调控Ⅰ型干扰素下游ISGs转录。本研究结果为深入探究PDCD10在抗病毒天然免疫中的作用积累了资料。The purpose of this study is to explore how the host protein programmed cell death factor 10(PDCD10)can inhibit the expression of typeⅠinterferon to promote the replication of foot-and-mouth disease virus(FMDV).First,this study verified the effect of overexpression and silencing of PDCD10 on FMDV replication.Secondly,the dual-luciferase reporter system was used to explore the effect of PDCD10 on the activation of typeⅠinterferon signaling pathway.Finally,real-time fluorescent quantitative PCR was used to explore the effect of PDCD10 on the transcription of stimulating genes downstream of the typeⅠinterferon pathway.The results showed that overexpression of PDCD10 significantly promoted FMDV replication while silencing PDCD10 significantly inhibited FMDV replication.Compared with the control,the cell culture supernatant infected with Sendai virus(SeV)after overexpression of PDCD10 significantly promoted FMDV replication.Furthermore,PDCD10 significantly inhibited the activation of IFN-βpromoter and NF-κB induced by SeV in a dose-dependent manner,and PDCD10 negatively regulated the transcription of typeⅠinterferon pathway signal molecules.Finally,it was found that PDCD10 negatively regulated the transcription of ISGs downstream of typeⅠinterferon.The results of this study have accumulated data for the in-depth exploration of the role of PDCD10 in antiviral innate immunity.

关 键 词：程序性细胞死亡因子10 PDCD10 FMDV Ⅰ型干扰素信号通路 IFN-Β 

分 类 号：S852.659.6[农业科学—基础兽医学]