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Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6C(low) and Ly6C(high)) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E(2) is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing r...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5338035/ https://www.ncbi.nlm.nih.gov/pubmed/28256515 http://dx.doi.org/10.1038/ncomms14656 |
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author | Tang, Juan Shen, Yujun Chen, Guilin Wan, Qiangyou Wang, Kai Zhang, Jian Qin, Jing Liu, Guizhu Zuo, Shengkai Tao, Bo Yu, Yu Wang, Junwen Lazarus, Michael Yu, Ying |
author_facet | Tang, Juan Shen, Yujun Chen, Guilin Wan, Qiangyou Wang, Kai Zhang, Jian Qin, Jing Liu, Guizhu Zuo, Shengkai Tao, Bo Yu, Yu Wang, Junwen Lazarus, Michael Yu, Ying |
author_sort | Tang, Juan |
collection | PubMed |
description | Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6C(low) and Ly6C(high)) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E(2) is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing remains to be determined. Here we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses accumulation of Ly6C(low) Mos/Mps in infarcted hearts. Ep3 deletion in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones. Ep3 deficiency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by suppressing TGFβ1 signalling and subsequently inhibits Ly6C(low) Mos/Mps migration and angiogenesis. Targeted overexpression of Ep3 receptors in Mos/Mps improves wound healing by enhancing angiogenesis. Thus, the PGE(2)/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6C(low) Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI. |
format | Online Article Text |
id | pubmed-5338035 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-53380352017-03-09 Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction Tang, Juan Shen, Yujun Chen, Guilin Wan, Qiangyou Wang, Kai Zhang, Jian Qin, Jing Liu, Guizhu Zuo, Shengkai Tao, Bo Yu, Yu Wang, Junwen Lazarus, Michael Yu, Ying Nat Commun Article Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6C(low) and Ly6C(high)) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E(2) is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing remains to be determined. Here we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses accumulation of Ly6C(low) Mos/Mps in infarcted hearts. Ep3 deletion in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones. Ep3 deficiency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by suppressing TGFβ1 signalling and subsequently inhibits Ly6C(low) Mos/Mps migration and angiogenesis. Targeted overexpression of Ep3 receptors in Mos/Mps improves wound healing by enhancing angiogenesis. Thus, the PGE(2)/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6C(low) Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI. Nature Publishing Group 2017-03-03 /pmc/articles/PMC5338035/ /pubmed/28256515 http://dx.doi.org/10.1038/ncomms14656 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Tang, Juan Shen, Yujun Chen, Guilin Wan, Qiangyou Wang, Kai Zhang, Jian Qin, Jing Liu, Guizhu Zuo, Shengkai Tao, Bo Yu, Yu Wang, Junwen Lazarus, Michael Yu, Ying Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction |
title | 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_short | 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 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5338035/ https://www.ncbi.nlm.nih.gov/pubmed/28256515 http://dx.doi.org/10.1038/ncomms14656 |
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