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

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 nucleo...

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Published in:Oncotarget 2016-11, Vol.7 (46), p.75064-75080
Main Authors: Huan, Chang-Chao, Wang, Hua-Xia, Sheng, Xiang-Xiang, Wang, Rui, Wang, Xin, Liao, Ying, Liu, Qin-Fang, Tong, Guang-Zhi, Ding, Chan, Fan, Hong-Jie, Wu, Jia-Qiang, Mao, Xiang
Format: Article
Language:English
Subjects:
Acetylation
Animals
Binding Sites
Biomarkers
CCAAT-Enhancer-Binding Protein-beta - metabolism
Cercopithecus aethiops
Coronavirus Infections - genetics
Coronavirus Infections - metabolism
Coronavirus Infections - virology
Cytokines - genetics
Cytokines - metabolism
Gene Expression Regulation
Histone Acetyltransferases - metabolism
HMGB1 Protein - genetics
HMGB1 Protein - metabolism
Inflammation Mediators - metabolism
NF-kappa B - metabolism
Nucleoproteins - metabolism
Nucleotide Motifs
Porcine epidemic diarrhea virus - physiology
Promoter Regions, Genetic
Protein Binding
Research Paper
Sirtuin 1 - metabolism
Transcription, Genetic
Vero Cells
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Summary: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.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.11991