Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages

Cardiomyocyte apoptosis in response to inflammation is a primary cause of myocardial ischemia-reperfusion injury (IRI). Nuclear factor erythroid 2 like 2 (Nrf2) reportedly plays an important role in myocardial IRI, but the underlying mechanism remains obscure. Expression data from the normal heart t...

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Autores principales:	Haijian Zhang, Yifei Liu, Xiaoqing Cao, Wenmiao Wang, Xiaohong Cui, Xuechao Yang, Yan Wang, Jiahai Shi
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	early myocardial ischemia-reperfusion Nrf2 Pdcd4 inflammation macrophages Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/2bb63b77ac9c41978be76e37a66aa616
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spelling	oai:doaj.org-article:2bb63b77ac9c41978be76e37a66aa6162021-12-01T15:27:43ZNrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages1664-322410.3389/fimmu.2021.763760https://doaj.org/article/2bb63b77ac9c41978be76e37a66aa6162021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.763760/fullhttps://doaj.org/toc/1664-3224Cardiomyocyte apoptosis in response to inflammation is a primary cause of myocardial ischemia-reperfusion injury (IRI). Nuclear factor erythroid 2 like 2 (Nrf2) reportedly plays an important role in myocardial IRI, but the underlying mechanism remains obscure. Expression data from the normal heart tissues of mice or heart tissues treated with reperfusion for 6 h after ischemia (IR6h) were acquired from the GEO database; changes in biological function and infiltrating immune cells were analyzed. The binding between the molecules was verified by chromatin immunoprecipitation sequencing. Based on confirmation that early myocardial ischemia-reperfusion (myocardial ischemia/reperfusion for 6 hours, IR6h) promoted myocardial apoptosis and inflammatory response, we found that Nrf2, cooperating with Programmed Cell Death 4, promoted transcription initiation of C-C Motif Chemokine Ligand 3 (Ccl3) in myocardial tissues of mice treated with IR6h. Moreover, Ccl3 contributed to the high signature score of C-C motif chemokine receptor 1 (Ccr1)-positive macrophages. The high signature score of Ccr1-positive macrophages leads to the release of pro-inflammatory factors interleukin 1 beta and interleukin 6. This study is the first to elucidate the damaging effect of Nrf2 via remodeling of the immune microenvironment in early myocardial ischemia-reperfusion, which provides us with new perspectives and treatment strategies for myocardial ischemia-reperfusion.Haijian ZhangHaijian ZhangYifei LiuXiaoqing CaoWenmiao WangXiaohong CuiXuechao YangYan WangJiahai ShiJiahai ShiFrontiers Media S.A.articleearly myocardial ischemia-reperfusionNrf2Pdcd4inflammationmacrophagesImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	early myocardial ischemia-reperfusion Nrf2 Pdcd4 inflammation macrophages Immunologic diseases. Allergy RC581-607
spellingShingle	early myocardial ischemia-reperfusion Nrf2 Pdcd4 inflammation macrophages Immunologic diseases. Allergy RC581-607 Haijian Zhang Haijian Zhang Yifei Liu Xiaoqing Cao Wenmiao Wang Xiaohong Cui Xuechao Yang Yan Wang Jiahai Shi Jiahai Shi Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages
description	Cardiomyocyte apoptosis in response to inflammation is a primary cause of myocardial ischemia-reperfusion injury (IRI). Nuclear factor erythroid 2 like 2 (Nrf2) reportedly plays an important role in myocardial IRI, but the underlying mechanism remains obscure. Expression data from the normal heart tissues of mice or heart tissues treated with reperfusion for 6 h after ischemia (IR6h) were acquired from the GEO database; changes in biological function and infiltrating immune cells were analyzed. The binding between the molecules was verified by chromatin immunoprecipitation sequencing. Based on confirmation that early myocardial ischemia-reperfusion (myocardial ischemia/reperfusion for 6 hours, IR6h) promoted myocardial apoptosis and inflammatory response, we found that Nrf2, cooperating with Programmed Cell Death 4, promoted transcription initiation of C-C Motif Chemokine Ligand 3 (Ccl3) in myocardial tissues of mice treated with IR6h. Moreover, Ccl3 contributed to the high signature score of C-C motif chemokine receptor 1 (Ccr1)-positive macrophages. The high signature score of Ccr1-positive macrophages leads to the release of pro-inflammatory factors interleukin 1 beta and interleukin 6. This study is the first to elucidate the damaging effect of Nrf2 via remodeling of the immune microenvironment in early myocardial ischemia-reperfusion, which provides us with new perspectives and treatment strategies for myocardial ischemia-reperfusion.
format	article
author	Haijian Zhang Haijian Zhang Yifei Liu Xiaoqing Cao Wenmiao Wang Xiaohong Cui Xuechao Yang Yan Wang Jiahai Shi Jiahai Shi
author_facet	Haijian Zhang Haijian Zhang Yifei Liu Xiaoqing Cao Wenmiao Wang Xiaohong Cui Xuechao Yang Yan Wang Jiahai Shi Jiahai Shi
author_sort	Haijian Zhang
title	Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages
title_short	Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages
title_full	Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages
title_fullStr	Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages
title_full_unstemmed	Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages
title_sort	nrf2 promotes inflammation in early myocardial ischemia-reperfusion via recruitment and activation of macrophages
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/2bb63b77ac9c41978be76e37a66aa616
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Nrf2 Promotes Inflammation in Early Myocardial Ischemia-Reperfusion via Recruitment and Activation of Macrophages

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