Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction

Acute myocardial infarction (AMI) triggers sterile inflammatory reaction mediated by prostaglandin E2 (PGE2). Tang et al. show that the PGE2 via its receptor EP3 promotes cardiac healing after AMI by recruiting reparative Ly6Clowmonocytes/macrophages, which is mediated by TGF-β-driven regulation of...

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Main Authors:	Juan Tang, Yujun Shen, Guilin Chen, Qiangyou Wan, Kai Wang, Jian Zhang, Jing Qin, Guizhu Liu, Shengkai Zuo, Bo Tao, Yu Yu, Junwen Wang, Michael Lazarus, Ying Yu
Format:	Article
Language:	English
Published:	Nature Publishing Group 2017-03-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/ncomms14656

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spelling	doaj-37060ae553b64255adedfaa4d80782982021-05-11T07:21:53ZengNature Publishing GroupNature Communications2041-17232017-03-018111410.1038/ncomms14656Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarctionJuan Tang0Yujun Shen1Guilin Chen2Qiangyou Wan3Kai Wang4Jian Zhang5Jing Qin6Guizhu Liu7Shengkai Zuo8Bo Tao9Yu Yu10Junwen Wang11Michael Lazarus12Ying Yu13Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesDepartment of Pharmacology, School of Basic Medical Sciences, Tianjin Medical UniversityDepartment of Pharmacology, School of Basic Medical Sciences, Tianjin Medical UniversityKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesCenter for Genomic Sciences, LKS Faculty of Medicine, The University of Hong KongKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesCenter for Genomic Sciences, LKS Faculty of Medicine, The University of Hong KongInternational Institute for Integrative Sleep Medicine (WPI-IIIS), University of TsukubaKey Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of SciencesAcute myocardial infarction (AMI) triggers sterile inflammatory reaction mediated by prostaglandin E2 (PGE2). Tang et al. show that the PGE2 via its receptor EP3 promotes cardiac healing after AMI by recruiting reparative Ly6Clowmonocytes/macrophages, which is mediated by TGF-β-driven regulation of CX3CR1 expression and VEGF secretion.https://doi.org/10.1038/ncomms14656
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Juan Tang Yujun Shen Guilin Chen Qiangyou Wan Kai Wang Jian Zhang Jing Qin Guizhu Liu Shengkai Zuo Bo Tao Yu Yu Junwen Wang Michael Lazarus Ying Yu
spellingShingle	Juan Tang Yujun Shen Guilin Chen Qiangyou Wan Kai Wang Jian Zhang Jing Qin Guizhu Liu Shengkai Zuo Bo Tao Yu Yu Junwen Wang Michael Lazarus Ying Yu Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction Nature Communications
author_facet	Juan Tang Yujun Shen Guilin Chen Qiangyou Wan Kai Wang Jian Zhang Jing Qin Guizhu Liu Shengkai Zuo Bo Tao Yu Yu Junwen Wang Michael Lazarus Ying Yu
author_sort	Juan Tang
title	Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
title_short	Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
title_full	Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
title_fullStr	Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
title_full_unstemmed	Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
title_sort	activation of e-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2017-03-01
description	Acute myocardial infarction (AMI) triggers sterile inflammatory reaction mediated by prostaglandin E2 (PGE2). Tang et al. show that the PGE2 via its receptor EP3 promotes cardiac healing after AMI by recruiting reparative Ly6Clowmonocytes/macrophages, which is mediated by TGF-β-driven regulation of CX3CR1 expression and VEGF secretion.
url	https://doi.org/10.1038/ncomms14656
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Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction

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