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 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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DOI：
10.3389/fphys.2021.780854
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发表时间：
2021
影响因子：
4
通讯作者：
Alcaide P
中科院分区：
文献类型：
--
作者：
Kaur K;Velázquez FE;Anastasiou M;Ngwenyama N;Smolgovsky S;Aronovitz M;Alcaide P
唾液粘蛋白 CD43 是一种在白细胞（包括先天性免疫细胞和适应性免疫细胞）中差异表达的跨膜蛋白。在多种细胞过程中，CD43 参与 T 细胞与血管内皮细胞的粘附，并有助于实验性自身免疫的进展。心脏中骨髓细胞和 T 细胞的连续浸润是心脏炎症和心力衰竭 (HF) 的标志。在此，我们报告 CD43−/− 小鼠对横主动脉缩窄 (TAC) 诱导的心力衰竭的存活率有所提高。与对照野生型 (WT) 小鼠相比，这种生存率的提高与收缩功能的改善、心脏纤维化的减少以及 TAC 响应下 T 细胞心脏浸润的显着减少有关。缺乏CD43并不会改变心脏中骨髓细胞的数量，但会导致心脏CXCL10（T细胞的趋化剂）表达减少，并在体外导致单核细胞转变为抗炎巨噬细胞。总的来说，这些发现揭示了 CD43 通过调节心脏 T 细胞炎症在压力超负荷诱导的心力衰竭的不良心脏重塑中发挥的新作用。
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.
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