CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction

Ischemia-reperfusion injury after the reopening of an occluded coronary artery is a major cause of cardiac damage and inflammation after acute myocardial infarction. The chemokine axis CCL20-CCR6 is a key player in various inflammatory processes, including atherosclerosis; however, its role in ische...

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Autores principales:	David Schumacher, Elisa A. Liehn, Anjana Singh, Adelina Curaj, Erwin Wijnands, Sergio A. Lira, Frank Tacke, Joachim Jankowski, Erik A.L. Biessen, Emiel P.C. van der Vorst
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	acute myocardial infarction ischemia-reperfusion injury chemokine receptors CCR6 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/49aff1fc90e644ce8c2814a7984b1834
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spelling	oai:doaj.org-article:49aff1fc90e644ce8c2814a7984b18342021-11-25T16:48:39ZCCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction10.3390/biomedicines91115322227-9059https://doaj.org/article/49aff1fc90e644ce8c2814a7984b18342021-10-01T00:00:00Zhttps://www.mdpi.com/2227-9059/9/11/1532https://doaj.org/toc/2227-9059Ischemia-reperfusion injury after the reopening of an occluded coronary artery is a major cause of cardiac damage and inflammation after acute myocardial infarction. The chemokine axis CCL20-CCR6 is a key player in various inflammatory processes, including atherosclerosis; however, its role in ischemia-reperfusion injury has remained elusive. Therefore, to gain more insight into the role of the CCR6 in acute myocardial infarction, we have studied cardiac injury after transient ligation of the left anterior descending coronary artery followed by reperfusion in <i>C</i><i>cr</i><i>6</i><i><sup>−/−</sup></i> mice and their respective C57Bl/6 wild-type controls. Surprisingly, <i>C</i><i>cr</i><i>6</i><i><sup>−/−</sup></i> mice demonstrated significantly reduced cardiac function and increased infarct sizes after ischemia/reperfusion. This coincided with a significant increase in cardiac inflammation, characterized by an accumulation of neutrophils and inflammatory macrophage accumulation. Chimeras with a bone marrow deficiency of CCR6 mirrored this adverse <i>C</i><i>cr</i><i>6</i><i><sup>−/−</sup></i> phenotype, while cardiac injury was unchanged in chimeras with stromal CCR6 deficiency. This study demonstrates that CCR6-dependent (bone marrow) cells exert a protective role in myocardial infarction and subsequent ischemia-reperfusion injury, supporting the notion that augmenting CCR6-dependent immune mechanisms represents an interesting therapeutic target.David SchumacherElisa A. LiehnAnjana SinghAdelina CurajErwin WijnandsSergio A. LiraFrank TackeJoachim JankowskiErik A.L. BiessenEmiel P.C. van der VorstMDPI AGarticleacute myocardial infarctionischemia-reperfusion injurychemokine receptorsCCR6Biology (General)QH301-705.5ENBiomedicines, Vol 9, Iss 1532, p 1532 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	acute myocardial infarction ischemia-reperfusion injury chemokine receptors CCR6 Biology (General) QH301-705.5
spellingShingle	acute myocardial infarction ischemia-reperfusion injury chemokine receptors CCR6 Biology (General) QH301-705.5 David Schumacher Elisa A. Liehn Anjana Singh Adelina Curaj Erwin Wijnands Sergio A. Lira Frank Tacke Joachim Jankowski Erik A.L. Biessen Emiel P.C. van der Vorst CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction
description	Ischemia-reperfusion injury after the reopening of an occluded coronary artery is a major cause of cardiac damage and inflammation after acute myocardial infarction. The chemokine axis CCL20-CCR6 is a key player in various inflammatory processes, including atherosclerosis; however, its role in ischemia-reperfusion injury has remained elusive. Therefore, to gain more insight into the role of the CCR6 in acute myocardial infarction, we have studied cardiac injury after transient ligation of the left anterior descending coronary artery followed by reperfusion in <i>C</i><i>cr</i><i>6</i><i><sup>−/−</sup></i> mice and their respective C57Bl/6 wild-type controls. Surprisingly, <i>C</i><i>cr</i><i>6</i><i><sup>−/−</sup></i> mice demonstrated significantly reduced cardiac function and increased infarct sizes after ischemia/reperfusion. This coincided with a significant increase in cardiac inflammation, characterized by an accumulation of neutrophils and inflammatory macrophage accumulation. Chimeras with a bone marrow deficiency of CCR6 mirrored this adverse <i>C</i><i>cr</i><i>6</i><i><sup>−/−</sup></i> phenotype, while cardiac injury was unchanged in chimeras with stromal CCR6 deficiency. This study demonstrates that CCR6-dependent (bone marrow) cells exert a protective role in myocardial infarction and subsequent ischemia-reperfusion injury, supporting the notion that augmenting CCR6-dependent immune mechanisms represents an interesting therapeutic target.
format	article
author	David Schumacher Elisa A. Liehn Anjana Singh Adelina Curaj Erwin Wijnands Sergio A. Lira Frank Tacke Joachim Jankowski Erik A.L. Biessen Emiel P.C. van der Vorst
author_facet	David Schumacher Elisa A. Liehn Anjana Singh Adelina Curaj Erwin Wijnands Sergio A. Lira Frank Tacke Joachim Jankowski Erik A.L. Biessen Emiel P.C. van der Vorst
author_sort	David Schumacher
title	CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction
title_short	CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction
title_full	CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction
title_fullStr	CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction
title_full_unstemmed	CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction
title_sort	ccr6 deficiency increases infarct size after murine acute myocardial infarction
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/49aff1fc90e644ce8c2814a7984b1834
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CCR6 Deficiency Increases Infarct Size after Murine Acute Myocardial Infarction

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