Reg3β from cardiomyocytes regulated macrophage migration, proliferation and functional skewing in experimental autoimmune myocarditis.

IF 1.4 Q4 IMMUNOLOGY American journal of clinical and experimental immunology Pub Date : 2018-04-05 eCollection Date: 2018-01-01
Shanshan Zhou, Han Jiang, Han Wang, Hongxiang Lu, Rong Chen, Huaxi Xu, Zhaoliang Su, Xiaoyi Shao
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Abstract

Macrophages play critical roles in inflammatory initiation, development, resolution and cardiac regeneration of myocarditis. However, Reg3β, as a member of regenerating family of proteins, contributes to dedifferentiation of injury cardiomyocytes as well as cardiac function remodeling. It remains unclear whether Reg3β was associated with macrophages reprogramming during autoimmune myocarditis. Our results showed that Reg3β could effectively recruit macrophages, promoted their proliferation and phagocytosis, and facilitated their polarized into M2 macrophages. Macrophage, especially M1 phenotype contributed to Reg3β production by cardiomyocytes. Our data also indicated that Reg3β was involved in self-protection mechanism following cardiac injury or stress. This suggests that Reg3β might be a critically protective factor of myocardium.

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来自心肌细胞的Reg3β调节实验性自身免疫性心肌炎中巨噬细胞的迁移、增殖和功能倾斜。
巨噬细胞在心肌炎的炎症发生、发展、消退和心脏再生中起着至关重要的作用。然而,Reg3β作为再生蛋白家族的一员,有助于损伤心肌细胞的去分化和心功能重塑。自身免疫性心肌炎期间,Reg3β是否与巨噬细胞重编程相关尚不清楚。结果表明,Reg3β能有效募集巨噬细胞,促进其增殖和吞噬,并促进其极化为M2巨噬细胞。巨噬细胞,特别是M1表型有助于心肌细胞产生Reg3β。我们的数据还表明Reg3β参与心脏损伤或应激后的自我保护机制。这提示Reg3β可能是心肌的关键保护因子。
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