Oncotarget

Research Papers:

Porcine epidemic diarrhea virus nucleoprotein contributes to HMGB1 transcription and release by interacting with C/EBP-β

Chang-chao Huan, Hua-xia Wang, Xiang-xiang Sheng, Rui Wang, Xin Wang, Ying Liao, Qin-fang Liu, Guang-zhi Tong, Chan Ding, Hong-jie Fan, Jia-qiang Wu and Xiang Mao _

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Oncotarget. 2016; 7:75064-75080. https://doi.org/10.18632/oncotarget.11991

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Abstract

Chang-chao Huan1, Hua-xia Wang1, Xiang-xiang Sheng1, Rui Wang1, Xin Wang1, Ying Liao2, Qin-fang Liu2, Guang-zhi Tong2, Chan Ding2, Hong-jie Fan1, Jia-qiang Wu3, Xiang Mao1,2

1College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province, China, 210095

2Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, China, 200241

3Institute of Animal Science and Veterinary Medicine, Shandong Academy of Agricultural Sciences, Shandong Province, China, 250100

Correspondence to:

Xiang Mao, email: xmao@njau.edu.cn, xmao@shvri.ac.cn

Keywords: porcine epidemic diarrhea virus, HMGB1, nucleoprotein, C/EBP-β

Received: May 09, 2016    Accepted: September 02, 2016    Published: September 13, 2016

ABSTRACT

Porcine epidemic diarrhea is a devastating swine enteric disease, which is caused by porcine epidemic diarrhea virus (PEDV) infection. Our studies demonstrated that PEDV infection resulted in the up-regulation of proinflammatory cytokines. Meanwhile, PEDV infection and overexpression of viral nucleoprotein resulted in the acetylation and release of high mobility group box 1 proteins in vitro, an important proinflammatory response mediator, which contributes to the pathogenesis of various inflammatory diseases. Our studies also showed that SIRT1, histone acetyltransferase, and NF-κB regulated the acetylation and release of HMGB1. Chromatin immunoprecipitation, dual-luciferase reporter gene assay, and co-immunoprecipitation experiments illustrated that PEDV-N could induce HMGB1 transcription by interacting with C/EBP-β, which could bind to C/EBP motif in HMGB1 promotor region. Collectively, our data indicate PEDV-N contributes to HMGB1 transcription and the subsequent release/acetylation of HMGB1 during PEDV infection.


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