S100A8/A9 drives the formation of procoagulant platelets through GPIbα.
Journal
Blood
ISSN: 1528-0020
Titre abrégé: Blood
Pays: United States
ID NLM: 7603509
Informations de publication
Date de publication:
15 12 2022
15 12 2022
Historique:
accepted:
09
08
2022
received:
29
11
2021
pubmed:
27
8
2022
medline:
20
12
2022
entrez:
26
8
2022
Statut:
ppublish
Résumé
S100A8/A9, also known as "calprotectin" or "MRP8/14," is an alarmin primarily secreted by activated myeloid cells with antimicrobial, proinflammatory, and prothrombotic properties. Increased plasma levels of S100A8/A9 in thrombo-inflammatory diseases are associated with thrombotic complications. We assessed the presence of S100A8/A9 in the plasma and lung autopsies from patients with COVID-19 and investigated the molecular mechanism by which S100A8/A9 affects platelet function and thrombosis. S100A8/A9 plasma levels were increased in patients with COVID-19 and sustained high levels during hospitalization correlated with poor outcomes. Heterodimeric S100A8/A9 was mainly detected in neutrophils and deposited on the vessel wall in COVID-19 lung autopsies. Immobilization of S100A8/A9 with collagen accelerated the formation of a fibrin-rich network after perfusion of recalcified blood at venous shear. In vitro, platelets adhered and partially spread on S100A8/A9, leading to the formation of distinct populations of either P-selectin or phosphatidylserine (PS)-positive platelets. By using washed platelets, soluble S100A8/A9 induced PS exposure but failed to induce platelet aggregation, despite GPIIb/IIIa activation and alpha-granule secretion. We identified GPIbα as the receptor for S100A8/A9 on platelets inducing the formation of procoagulant platelets with a supporting role for CD36. The effect of S100A8/A9 on platelets was abolished by recombinant GPIbα ectodomain, platelets from a patient with Bernard-Soulier syndrome with GPIb-IX-V deficiency, and platelets from mice deficient in the extracellular domain of GPIbα. We identified the S100A8/A9-GPIbα axis as a novel targetable prothrombotic pathway inducing procoagulant platelets and fibrin formation, in particular in diseases associated with high levels of S100A8/A9, such as COVID-19.
Identifiants
pubmed: 36026606
pii: S0006-4971(22)01113-2
doi: 10.1182/blood.2021014966
pmc: PMC10653093
doi:
Substances chimiques
Calgranulin A
0
Fibrin
9001-31-4
Phosphatidylserines
0
S100A9 protein, human
0
Calgranulin B
0
adhesion receptor
0
Platelet Glycoprotein GPIb-IX Complex
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2626-2643Subventions
Organisme : British Heart Foundation
ID : PG/21/10737
Pays : United Kingdom
Organisme : British Heart Foundation
ID : AA/18/2/34218
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 204951
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/IBSRF/20/25039
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH03/003
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_19029
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH/03/003/15571
Pays : United Kingdom
Informations de copyright
© 2022 by The American Society of Hematology.
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