TRIF promotes angiotensin II-induced cross-talk between fibroblasts and macrophages in atrial fibrosis

Journal Article · Fri Aug 14 00:00:00 EDT 2015 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2015.05.131· OSTI ID:22462177

Chen, Xiao-Qing; Zhang, Dao-Liang ^[1]; Zhang, Ming-Jian; Guo, Meng; Zhan, Yang-Yang; Liu, Fang ^[2]; Jiang, Wei-Feng; Zhou, Li ^[1]; Zhao, Liang ^[1]; Wang, Quan-Xing ^[2]; Liu, Xu ^[1]

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1. Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai (China)
2. National Key Laboratory of Medical Immunology, Second Military Medical University, Shanghai (China)

Aims: Atrial fibroblasts and macrophages have long been thought to participate in atrial fibrillation (AF). However, which specific mediator may regulate the interaction between them remains unclear. Methods and results: We provided the evidence for the involvement of Toll/IL-1 receptor domain-containing adaptor inducing IFN-β (TRIF), an important inflammation-related molecule, in the pathophysiology of AF. Patients with AF showed higher levels of angiotensin II (AngII) and TRIF expression and larger number of macrophages infiltration in left atria appendage than individuals with sinus rhythm (SR). In the cell study, AngII induced chemokines expressions in mouse atrial fibroblasts and AngII-stimulated atrial fibroblasts induced the chemotaxis of macrophages, which were reduced by losartan and TRIF siRNA. Meanwhile, AngII-stimulated atrial fibroblasts proliferation was enhanced by macrophages. Conclusions: Our data demonstrated that TRIF may be a crucial factor promoting the interaction between atrial fibroblasts and macrophages, leading to atrial fibrosis. - Highlights: • Compared with SR, AF showed higher TRIF expression in left atrial appendage. • TRIF siRNA reversed macrophage chemotaxis induced by AngII-treated fibroblast. • TRIF siRNA reversed chemokines expressions induced by AngII in fibroblast. • AngII-stimulated atrial fibroblast proliferation was enhanced by macrophage.

• OSTI ID: 22462177
• Journal Information: Biochemical and Biophysical Research Communications, Vol. 464, Issue 1; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANGIOTENSIN
ATRIA
FIBROBLASTS
FIBROSIS
INFLAMMATION
MACROPHAGES
MICE
PATIENTS
RADIOPROTECTIVE SUBSTANCES
RECEPTORS
SINUSES