A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.

<h4>Background</h4>Viral myocarditis, which is most prevalently caused by Coxsackievirus B3 (CVB3) infection, is a serious clinical condition characterized by cardiac inflammation. However, efficient therapies targeting inflammation are still lacking and much needed. A20, also known as t...

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Autores principales:	Jun Gui, Yan Yue, Ruizhen Chen, Wei Xu, Sidong Xiong
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c00d753cc25a45b5a4ea41a5fc9a2e90
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spelling	oai:doaj.org-article:c00d753cc25a45b5a4ea41a5fc9a2e902021-11-18T08:13:37ZA20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.1932-620310.1371/journal.pone.0046515https://doaj.org/article/c00d753cc25a45b5a4ea41a5fc9a2e902012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23029542/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Viral myocarditis, which is most prevalently caused by Coxsackievirus B3 (CVB3) infection, is a serious clinical condition characterized by cardiac inflammation. However, efficient therapies targeting inflammation are still lacking and much needed. A20, also known as tumor necrosis factor alpha induced protein 3 (TNFAIP3) is a key negative regulator of inflammation. But whether A20 may affect cardiac inflammation during acute viral myocarditis remains to be elucidated. The aim of this study was to investigate the potential protective effect of A20 on CVB3-induced myocarditis.<h4>Methodology/principal findings</h4>Mice were intraperitoneally inoculated with CVB3 to establish acute viral myocarditis model. We found that the expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and monocyte chemotactic protein-1 (MCP-1) were markedly and persistently increased during the progression of CVB3-induced myocarditis, and positively correlated with the disease severity. Notably, intravenous injection in vivo with adenovirus expressed A20 (Ad-A20) remarkably reduced CVB3-induced pro-inflammatory cytokines production and alleviated the severity of myocarditis. Further, we observed that nuclear factor-kappaB (NF-κB) signaling which mediates inflammatory response was significantly inhibited in CVB3-infected mice with Ad-A20 treatment. Finally, we revealed that A20 was required to inhibit CVB3-induced NF-κB signaling by restricting TNF receptor associated factor 6 (TRAF6) ubiquitylation.<h4>Conclusion/significance</h4>This study demonstrates the protective role of A20 against CVB3-induced myocarditis, which may provide a new therapeutic strategy for the treatment of viral myocarditis.Jun GuiYan YueRuizhen ChenWei XuSidong XiongPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e46515 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jun Gui Yan Yue Ruizhen Chen Wei Xu Sidong Xiong A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.
description	<h4>Background</h4>Viral myocarditis, which is most prevalently caused by Coxsackievirus B3 (CVB3) infection, is a serious clinical condition characterized by cardiac inflammation. However, efficient therapies targeting inflammation are still lacking and much needed. A20, also known as tumor necrosis factor alpha induced protein 3 (TNFAIP3) is a key negative regulator of inflammation. But whether A20 may affect cardiac inflammation during acute viral myocarditis remains to be elucidated. The aim of this study was to investigate the potential protective effect of A20 on CVB3-induced myocarditis.<h4>Methodology/principal findings</h4>Mice were intraperitoneally inoculated with CVB3 to establish acute viral myocarditis model. We found that the expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and monocyte chemotactic protein-1 (MCP-1) were markedly and persistently increased during the progression of CVB3-induced myocarditis, and positively correlated with the disease severity. Notably, intravenous injection in vivo with adenovirus expressed A20 (Ad-A20) remarkably reduced CVB3-induced pro-inflammatory cytokines production and alleviated the severity of myocarditis. Further, we observed that nuclear factor-kappaB (NF-κB) signaling which mediates inflammatory response was significantly inhibited in CVB3-infected mice with Ad-A20 treatment. Finally, we revealed that A20 was required to inhibit CVB3-induced NF-κB signaling by restricting TNF receptor associated factor 6 (TRAF6) ubiquitylation.<h4>Conclusion/significance</h4>This study demonstrates the protective role of A20 against CVB3-induced myocarditis, which may provide a new therapeutic strategy for the treatment of viral myocarditis.
format	article
author	Jun Gui Yan Yue Ruizhen Chen Wei Xu Sidong Xiong
author_facet	Jun Gui Yan Yue Ruizhen Chen Wei Xu Sidong Xiong
author_sort	Jun Gui
title	A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.
title_short	A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.
title_full	A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.
title_fullStr	A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.
title_full_unstemmed	A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.
title_sort	a20 (tnfaip3) alleviates cvb3-induced myocarditis via inhibiting nf-κb signaling.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/c00d753cc25a45b5a4ea41a5fc9a2e90
work_keys_str_mv	AT jungui a20tnfaip3alleviatescvb3inducedmyocarditisviainhibitingnfkbsignaling AT yanyue a20tnfaip3alleviatescvb3inducedmyocarditisviainhibitingnfkbsignaling AT ruizhenchen a20tnfaip3alleviatescvb3inducedmyocarditisviainhibitingnfkbsignaling AT weixu a20tnfaip3alleviatescvb3inducedmyocarditisviainhibitingnfkbsignaling AT sidongxiong a20tnfaip3alleviatescvb3inducedmyocarditisviainhibitingnfkbsignaling
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A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.

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