CD69 Plays a Beneficial Role in Ischemic Stroke by Dampening Endothelial Activation.
Animals
Antigens, CD
/ genetics
Antigens, Differentiation, T-Lymphocyte
/ genetics
Blood Coagulation
Blood Platelets
/ metabolism
Brain
/ blood supply
Cells, Cultured
DNA-Binding Proteins
/ deficiency
Disease Models, Animal
Endothelial Cells
/ metabolism
Infarction, Middle Cerebral Artery
/ genetics
Lectins, C-Type
/ deficiency
Lymphocyte Activation
Male
Mice, Inbred BALB C
Mice, Inbred C57BL
Signal Transduction
T-Lymphocytes
/ metabolism
von Willebrand Factor
/ metabolism
blood vessels
brain ischemia
endothelium
thrombosis
von Willebrand factor
Journal
Circulation research
ISSN: 1524-4571
Titre abrégé: Circ Res
Pays: United States
ID NLM: 0047103
Informations de publication
Date de publication:
18 01 2019
18 01 2019
Historique:
pubmed:
26
12
2018
medline:
19
11
2019
entrez:
25
12
2018
Statut:
ppublish
Résumé
CD69 is an immunomodulatory molecule induced during lymphocyte activation. Following stroke, T-lymphocytes upregulate CD69 but its function is unknown. We investigated whether CD69 was involved in brain damage following an ischemic stroke. We used adult male mice on the C57BL/6 or BALB/c backgrounds, including wild-type mice and CD69 CD69 deficiency promotes a prothrombotic phenotype characterized by increased VWF and worse brain damage after ischemic stroke. The results suggest that CD69 acts as a downregulator of endothelial activation.
Identifiants
pubmed: 30582456
doi: 10.1161/CIRCRESAHA.118.313818
doi:
Substances chimiques
Antigens, CD
0
Antigens, Differentiation, T-Lymphocyte
0
CD69 antigen
0
DNA-Binding Proteins
0
Lectins, C-Type
0
Rag2 protein, mouse
0
von Willebrand Factor
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM