CCN1/CYR61-mediated meticulous patrolling by Ly6Clow monocytes fuels vascular inflammation.

Détails

ID Serval
serval:BIB_F443DC13096D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
CCN1/CYR61-mediated meticulous patrolling by Ly6Clow monocytes fuels vascular inflammation.
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur⸱e⸱s
Imhof B.A., Jemelin S., Ballet R., Vesin C., Schapira M., Karaca M., Emre Y.
ISSN
1091-6490 (Electronic)
ISSN-L
0027-8424
Statut éditorial
Publié
Date de publication
16/08/2016
Peer-reviewed
Oui
Volume
113
Numéro
33
Pages
E4847-56
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Inflammation is characterized by the recruitment of leukocytes from the bloodstream. The rapid arrival of neutrophils is followed by a wave of inflammatory lymphocyte antigen 6 complex (Ly6C)-positive monocytes. In contrast Ly6C(low) monocytes survey the endothelium in the steady state, but their role in inflammation is still unclear. Here, using confocal intravital microscopy, we show that upon Toll-like receptor 7/8 (TLR7/8)-mediated inflammation of mesenteric veins, platelet activation drives the rapid mobilization of Ly6C(low) monocytes to the luminal side of the endothelium. After repeatedly interacting with platelets, Ly6C(low) monocytes commit to a meticulous patrolling of the endothelial wall and orchestrate the subsequent arrival and extravasation of neutrophils through the production of proinflammatory cytokines and chemokines. At a molecular level, we show that cysteine-rich protein 61 (CYR61)/CYR61 connective tissue growth factor nephroblastoma overexpressed 1 (CCN1) protein is released by activated platelets and enables the recruitment of Ly6C(low) monocytes upon vascular inflammation. In addition endothelium-bound CCN1 sustains the adequate patrolling of Ly6C(low) monocytes both in the steady state and under inflammatory conditions. Blocking CCN1 or platelets with specific antibodies impaired the early arrival of Ly6C(low) monocytes and abolished the recruitment of neutrophils. These results refine the leukocyte recruitment cascade model by introducing endothelium-bound CCN1 as an inflammation mediator and by demonstrating a role for platelets and patrolling Ly6C(low) monocytes in acute vascular inflammation.
Mots-clé
Animals, Antigens, Ly/analysis, Blood Platelets/physiology, Cell Movement, Cysteine-Rich Protein 61/physiology, Mice, Mice, Inbred C57BL, Monocytes/physiology, Neutrophils/physiology, Toll-Like Receptor 7/physiology, Toll-Like Receptor 8/physiology, Vasculitis/etiology, CCN1, inflammation, monocyte, neutrophil, platelet
Pubmed
Web of science
Open Access
Oui
Création de la notice
27/04/2023 21:59
Dernière modification de la notice
28/04/2023 5:54
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