CaMKII versus DAPK1 Binding to GluN2B in Ischemic Neuronal Cell Death after Resuscitation from Cardiac Arrest.
Animals
Calcium-Calmodulin-Dependent Protein Kinase Type 2
/ metabolism
Cell Death
/ drug effects
Death-Associated Protein Kinases
/ metabolism
Dendritic Spines
/ drug effects
Female
Glutamic Acid
/ toxicity
HEK293 Cells
Heart Arrest
/ metabolism
Humans
Ischemia
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mutation
/ genetics
Neuroprotection
/ drug effects
Neuroprotective Agents
/ pharmacology
Neurotoxins
/ toxicity
Protein Binding
/ drug effects
Rats, Sprague-Dawley
Receptors, N-Methyl-D-Aspartate
/ genetics
Resuscitation
CaMKII
DAPK1
GluN2B
cardiac arrest
cardiopulmonary resuscitation
excitotoxicity
hippocampus
ischemia
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
07 01 2020
07 01 2020
Historique:
received:
03
07
2019
revised:
25
09
2019
accepted:
19
11
2019
entrez:
9
1
2020
pubmed:
9
1
2020
medline:
7
1
2021
Statut:
ppublish
Résumé
DAPK1 binding to GluN2B was prominently reported to mediate ischemic cell death in vivo. DAPK1 and CaMKII bind to the same GluN2B region, and their binding is mutually exclusive. Here, we show that mutating the binding region on GluN2B (L1298A/R1300Q) protected against neuronal cell death induced by cardiac arrest followed by resuscitation. Importantly, the GluN2B mutation selectively abolished only CaMKII, but not DAPK1, binding. During ischemic or excitotoxic insults, CaMKII further accumulated at excitatory synapses, and this accumulation was mediated by GluN2B binding. Interestingly, extra-synaptic GluN2B decreased after ischemia, but its relative association with DAPK1 increased. Thus, ischemic neuronal death requires CaMKII binding to synaptic GluN2B, whereas any potential role for DAPK1 binding is restricted to a different, likely extra-synaptic population of GluN2B.
Identifiants
pubmed: 31914378
pii: S2211-1247(19)31567-0
doi: 10.1016/j.celrep.2019.11.076
pmc: PMC6959131
mid: NIHMS1548570
pii:
doi:
Substances chimiques
NR2B NMDA receptor
0
Neuroprotective Agents
0
Neurotoxins
0
Receptors, N-Methyl-D-Aspartate
0
Glutamic Acid
3KX376GY7L
Dapk1 protein, mouse
EC 2.7.11.1
Death-Associated Protein Kinases
EC 2.7.11.1
Calcium-Calmodulin-Dependent Protein Kinase Type 2
EC 2.7.11.17
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-8.e4Subventions
Organisme : NIA NIH HHS
ID : F31 AG062160
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS081248
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS080851
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007635
Pays : United States
Organisme : NINDS NIH HHS
ID : F31 NS092265
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS118786
Pays : United States
Organisme : NIA NIH HHS
ID : T32 AG000279
Pays : United States
Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
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