Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis

Sialomucin CD43 is a transmembrane protein differentially expressed in leukocytes that include innate and adaptive immune cells. Among a variety of cellular processes, CD43 participates in T cell adhesion to vascular endothelial cells and contributes to the progression of experimental autoimmunity....

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Autores principales:	Kuljeet Kaur, Francisco E. Velázquez, Marina Anastasiou, Njabulo Ngwenyama, Sasha Smolgovsky, Mark Aronovitz, Pilar Alcaide
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	heart failure inflammation CD43 T cell CXCL10 Physiology QP1-981
Acceso en línea:	https://doaj.org/article/144ebefa59894a3a9556ef207477efe0
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spelling	oai:doaj.org-article:144ebefa59894a3a9556ef207477efe02021-12-03T06:11:51ZSialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis1664-042X10.3389/fphys.2021.780854https://doaj.org/article/144ebefa59894a3a9556ef207477efe02021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.780854/fullhttps://doaj.org/toc/1664-042XSialomucin CD43 is a transmembrane protein differentially expressed in leukocytes that include innate and adaptive immune cells. Among a variety of cellular processes, CD43 participates in T cell adhesion to vascular endothelial cells and contributes to the progression of experimental autoimmunity. Sequential infiltration of myeloid cells and T cells in the heart is a hallmark of cardiac inflammation and heart failure (HF). Here, we report that CD43−/− mice have improved survival to HF induced by transverse aortic constriction (TAC). This enhanced survival is associated with improved systolic function, decreased cardiac fibrosis, and significantly reduced T cell cardiac infiltration in response to TAC compared to control wild-type (WT) mice. Lack of CD43 did not alter the number of myeloid cells in the heart, but resulted in decreased cardiac CXCL10 expression, a chemoattractant for T cells, and in a monocyte shift to anti-inflammatory macrophages in vitro. Collectively, these findings unveil a novel role for CD43 in adverse cardiac remodeling in pressure overload induced HF through modulation of cardiac T cell inflammation.Kuljeet KaurFrancisco E. VelázquezMarina AnastasiouMarina AnastasiouNjabulo NgwenyamaSasha SmolgovskyMark AronovitzPilar AlcaidePilar AlcaideFrontiers Media S.A.articleheart failureinflammationCD43T cellCXCL10PhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	heart failure inflammation CD43 T cell CXCL10 Physiology QP1-981
spellingShingle	heart failure inflammation CD43 T cell CXCL10 Physiology QP1-981 Kuljeet Kaur Francisco E. Velázquez Marina Anastasiou Marina Anastasiou Njabulo Ngwenyama Sasha Smolgovsky Mark Aronovitz Pilar Alcaide Pilar Alcaide Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis
description	Sialomucin CD43 is a transmembrane protein differentially expressed in leukocytes that include innate and adaptive immune cells. Among a variety of cellular processes, CD43 participates in T cell adhesion to vascular endothelial cells and contributes to the progression of experimental autoimmunity. Sequential infiltration of myeloid cells and T cells in the heart is a hallmark of cardiac inflammation and heart failure (HF). Here, we report that CD43−/− mice have improved survival to HF induced by transverse aortic constriction (TAC). This enhanced survival is associated with improved systolic function, decreased cardiac fibrosis, and significantly reduced T cell cardiac infiltration in response to TAC compared to control wild-type (WT) mice. Lack of CD43 did not alter the number of myeloid cells in the heart, but resulted in decreased cardiac CXCL10 expression, a chemoattractant for T cells, and in a monocyte shift to anti-inflammatory macrophages in vitro. Collectively, these findings unveil a novel role for CD43 in adverse cardiac remodeling in pressure overload induced HF through modulation of cardiac T cell inflammation.
format	article
author	Kuljeet Kaur Francisco E. Velázquez Marina Anastasiou Marina Anastasiou Njabulo Ngwenyama Sasha Smolgovsky Mark Aronovitz Pilar Alcaide Pilar Alcaide
author_facet	Kuljeet Kaur Francisco E. Velázquez Marina Anastasiou Marina Anastasiou Njabulo Ngwenyama Sasha Smolgovsky Mark Aronovitz Pilar Alcaide Pilar Alcaide
author_sort	Kuljeet Kaur
title	Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis
title_short	Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis
title_full	Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis
title_fullStr	Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis
title_full_unstemmed	Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis
title_sort	sialomucin cd43 plays a deleterious role in the development of experimental heart failure induced by pressure overload by modulating cardiac inflammation and fibrosis
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/144ebefa59894a3a9556ef207477efe0
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Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis

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