Kruppel-like factor 10 protects against acute viral myocarditis by negatively regulating cardiac MCP-1 expression

查看全文 作　　者：Jie [1]Yang;Hongkai [1]Zhang;Xuelian [2]Wang;Jing [2]Guo;Lin [1]Wei;Yahui [1]Song;Yuan [1]Luo;YinXia [3]Zhao;Malayannan [4]Subramaniam;Thomas [4]C.Spelsberg;Lie [2]Wang;Wei [1]Xu;Min [1]Li

机构地区：[1]Institute of Biology and Medical Sciences,Soochow University,Building 703,199 Ren-ai Road,215123,Suzhou,China;[2]Institute of Immunology,Zhejiang University School of Medicine,Hangzhou,China;[3]Central Laboratory,Shanghai Xuhui Central Hospital,Zhongshan-Xuhui Hospital,Fudan University,200031,Shanghai,China;[4]Department of Biochemistry and Molecular Biology,Mayo Clinic,Rochester,MN,USA

出　　处：《Cellular & Molecular Immunology》索引2021年第18卷第9期,共13页

基　　金：This work was supported by the Chinese National Natural Science Foundation(31400769,31870903,31870868,and 31670930);Jiangsu Province Natural Science Foundation(BK20140371);Jiangsu Postdoctoral Science Foundation(1402176C);Priority Academic Program Development of Jiangsu Higher Education Institutions. 摘　　要：Viral myocarditis(VMC)is a cardiac disease associated with myocardial inflammation and injury induced by virus infection.Cardiomyocytes have recently been regarded as key players in eliciting and modulating inflammation within the myocardium.Kruppel-like factor 10(KLF10)is a crucial regulator of various pathological processes and plays different roles in a variety of diseases.However,its role in VMC induced by coxsackievirus B3(CVB3)infection remains unknown.In this study,we report that cardiac KLF10 confers enhanced protection against viral myocarditis.We found that KLF10 expression was downregulated upon CVB3 infection.KLF10 deficiency enhanced cardiac viral replication and aggravated VMC progress.Bone marrow chimera experiments indicated that KLF10 expression in nonhematopoietic cells was involved in the pathogenesis of VMC.We further identified MCP-1 as a novel target of KLF10 in cardiomyocytes,and KLF10 cooperated with histone deacetylase 1(HDAC1)to negatively regulate MCP-1 expression by binding its promoter,leading to activation of MCP-1 transcription and recruitment of Ly6C^(high) monocytes/macrophages into the myocardium.This novel mechanism of MCP-1 regulation by KLF10 might provide new insights into the pathogenesis of VMC and a potential therapeutic target for VMC. 关键词：Kruppel-like factor 10 coxsackievirus B MYOCARDITIS INFLAMMATION MCP-1

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Kruppel-like factor 10 protects against acute viral myocarditis by negatively regulating cardiac MCP-1 expression

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