Brothers in arms: platelets and neutrophils in ischemic stroke.
Journal
Current opinion in hematology
ISSN: 1531-7048
Titre abrégé: Curr Opin Hematol
Pays: United States
ID NLM: 9430802
Informations de publication
Date de publication:
01 09 2021
01 09 2021
Historique:
pubmed:
30
6
2021
medline:
18
9
2021
entrez:
29
6
2021
Statut:
ppublish
Résumé
In this review, we will describe how the combined ability of platelets and neutrophils to interact with each other drives ischemic stroke brain injury. Neutrophils are one of the first cells to respond during ischemic stroke. Although animals stroke models have indicated targeting neutrophils improves outcomes, clinical trials have failed to yield successful strategies. Platelets play a critical role in recruiting neutrophils to sites of injury by acting as a bridge to the injured endothelium. After initial platelet adhesion, neutrophils can rapidly bind platelets through P-selectin and glycoprotein Ibα. In addition, recent data implicated platelet phosphatidylserine as a novel key regulator of platelet-neutrophil interactions in the setting of ischemic stroke. Inhibition of procoagulant platelets decreases circulating platelet-neutrophil aggregates and thereby reduces infarct size. Platelet binding alters neutrophil function, which contributes to the injury associated with ischemic stroke. This includes inducing the release of neutrophil extracellular traps, which are neurotoxic and pro-thrombotic, leading to impaired stroke outcomes. Platelet-neutrophil interactions significantly contribute to the pathophysiology of ischemic stroke brain injury. Better understanding the mechanisms behind their formation and the downstream consequences of their interactions will lead to improved therapies for stroke patients.
Identifiants
pubmed: 34183536
doi: 10.1097/MOH.0000000000000665
pii: 00062752-202109000-00004
pmc: PMC8483595
mid: NIHMS1717493
doi:
Substances chimiques
P-Selectin
0
Platelet Glycoprotein GPIb-IX Complex
0
SELP protein, human
0
adhesion receptor
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
301-307Subventions
Organisme : NIA NIH HHS
ID : K01 AG059892
Pays : United States
Organisme : NINDS NIH HHS
ID : U24 NS107228
Pays : United States
Informations de copyright
Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.
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