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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.
- Source :
- Frontiers in Physiology; 12/3/2021, Vol. 12, p1-10, 10p
- Publication Year :
- 2021
-
Abstract
- 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. [ABSTRACT FROM AUTHOR]
- Subjects :
- MYELOID cells
HEART fibrosis
VASCULAR endothelial cells
HEART cells
HEART failure
Subjects
Details
- Language :
- English
- ISSN :
- 1664042X
- Volume :
- 12
- Database :
- Complementary Index
- Journal :
- Frontiers in Physiology
- Publication Type :
- Academic Journal
- Accession number :
- 153972871
- Full Text :
- https://doi.org/10.3389/fphys.2021.780854