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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
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....
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8678270/ https://www.ncbi.nlm.nih.gov/pubmed/34925069 http://dx.doi.org/10.3389/fphys.2021.780854 |
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author | Kaur, Kuljeet Velázquez, Francisco E. Anastasiou, Marina Ngwenyama, Njabulo Smolgovsky, Sasha Aronovitz, Mark Alcaide, Pilar |
author_facet | Kaur, Kuljeet Velázquez, Francisco E. Anastasiou, Marina Ngwenyama, Njabulo Smolgovsky, Sasha Aronovitz, Mark Alcaide, Pilar |
author_sort | Kaur, Kuljeet |
collection | PubMed |
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 | Online Article Text |
id | pubmed-8678270 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86782702021-12-18 Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis Kaur, Kuljeet Velázquez, Francisco E. Anastasiou, Marina Ngwenyama, Njabulo Smolgovsky, Sasha Aronovitz, Mark Alcaide, Pilar Front Physiol Physiology 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. Frontiers Media S.A. 2021-12-03 /pmc/articles/PMC8678270/ /pubmed/34925069 http://dx.doi.org/10.3389/fphys.2021.780854 Text en Copyright © 2021 Kaur, Velázquez, Anastasiou, Ngwenyama, Smolgovsky, Aronovitz and Alcaide. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Physiology Kaur, Kuljeet Velázquez, Francisco E. Anastasiou, Marina Ngwenyama, Njabulo Smolgovsky, Sasha Aronovitz, Mark Alcaide, Pilar Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis |
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_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_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_sort | sialomucin cd43 plays a deleterious role in the development of experimental heart failure induced by pressure overload by modulating cardiac inflammation and fibrosis |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8678270/ https://www.ncbi.nlm.nih.gov/pubmed/34925069 http://dx.doi.org/10.3389/fphys.2021.780854 |
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