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

• Published in: Frontiers in physiology Vol. 12; p. 780854
• Main Authors: Kaur, Kuljeet, Velázquez, Francisco E, Anastasiou, Marina, Ngwenyama, Njabulo, Smolgovsky, Sasha, Aronovitz, Mark, Alcaide, Pilar
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 03-12-2021
• Subjects: CD43; CXCL10; heart failure; inflammation; Physiology; T cell; CXCL10; heart failure; inflammation; T cell; CD43
• ISSN: 1664-042X; 1664-042X
• DOI: 10.3389/fphys.2021.780854

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
. 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.