EphB2-dependent signaling promotes neuronal excitotoxicity and inflammation in the acute phase of ischemic stroke.
EphB2
Ephrin-B2
Excitotoxicity
Inflammation
Ischemic stroke
NMDA
Journal
Acta neuropathologica communications
ISSN: 2051-5960
Titre abrégé: Acta Neuropathol Commun
Pays: England
ID NLM: 101610673
Informations de publication
Date de publication:
05 02 2019
05 02 2019
Historique:
received:
11
12
2018
accepted:
28
01
2019
entrez:
7
2
2019
pubmed:
7
2
2019
medline:
3
4
2020
Statut:
epublish
Résumé
Local cerebral hypoperfusion causes ischemic stroke while driving multiple cell-specific responses including inflammation, glutamate-induced neurotoxicity mediated via NMDAR, edema formation and angiogenesis. Despite the relevance of these pathophysiological mechanisms for disease progression and outcome, molecular determinants controlling the onset of these processes are only partially understood. In this context, our study intended to investigate the functional role of EphB2, a receptor tyrosine kinase that is crucial for synapse function and binds to membrane-associated ephrin-B ligands.Cerebral ischemia was induced in Ephb2
Identifiants
pubmed: 30722785
doi: 10.1186/s40478-019-0669-7
pii: 10.1186/s40478-019-0669-7
pmc: PMC6362601
doi:
Substances chimiques
Ephb2 protein, mouse
EC 2.7.10.1
Receptor, EphB2
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
15Subventions
Organisme : Deutsche Forschungsgemeinschaft DFG
ID : MA 2240/5-2
Pays : International
Organisme : Deutsche Forschungsgemeinschaft DFG
ID : KO 2344/5-2
Pays : International
Organisme : Deutsche Forschungsgemeinschaft DFG
ID : SFB 1158 A05
Pays : International
Organisme : Deutsche Forschungsgemeinschaft DFG
ID : DIP BA 1007/7-1
Pays : International
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