Atrial epicardial adipose tissue abundantly secretes myeloperoxidase and activates atrial fibroblasts in patients with atrial fibrillation

Autor: Eva R. Meulendijks, Rushd F. M. Al-Shama, Makiri Kawasaki, Benedetta Fabrizi, Jolien Neefs, Robin Wesselink, Auriane C. Ernault, Sander Piersma, Thang V. Pham, Connie R. Jimenez, Jaco C. Knol, Wim J. P. van Boven, Antoine H. G. Driessen, Tim A. C. de Vries, Britt van der Leeden, Hans W. M. Niessen, Onno J. de Boer, Sébastien P. J. Krul, Joris R. de Groot
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: Journal of Translational Medicine, Vol 21, Iss 1, Pp 1-14 (2023)
Druh dokumentu: article
ISSN: 1479-5876
DOI: 10.1186/s12967-023-04231-2
Popis: Abstract Background Epicardial adipose tissue (EAT) secretome induces fibrosis. Fibrosis, primarily extracellular matrix (ECM) produced by fibroblasts, creates a substrate for atrial fibrillation (AF). Whether the EAT secretome from patients with AF activates human atrial fibroblasts and through which components, remains unexplored. Research aims (a) To investigate if the EAT secretome from patients with versus without AF increases ECM production in atrial fibroblasts. (b) To identify profibrotic proteins and processes in the EAT secretome and EAT from patients with, who will develop (future onset), and without AF. Methods Atrial EAT was obtainded during thoracoscopic ablation (AF, n = 20), or open-heart surgery (future onset and non-AF, n = 35). ECM gene expression of human atrial fibroblasts exposed to the EAT secretome and the proteomes of EAT secretome and EAT were assessed in patients with and without AF. Myeloperoxidase and neutrophil extracellular traps (NETs) were assessed immunohistochemically in patients with paroxysmal, persistent, future onset, and those who remain free of AF (non-AF). Results The expression of COL1A1 and FN1 in fibroblasts exposed to secretome from patients with AF was 3.7 and 4.7 times higher than in patients without AF (p
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