Inhibition of Calcium/Calmodulin-Dependent Protein Kinase Kinase β Is Detrimental in Hypoxia⁻Ischemia Neonatal Brain Injury.
Animals
Animals, Newborn
Benzimidazoles
/ pharmacology
Blood-Brain Barrier
/ drug effects
Blotting, Western
Calcium-Calmodulin-Dependent Protein Kinase Kinase
/ antagonists & inhibitors
Cell Death
/ drug effects
Hypoxia-Ischemia, Brain
/ enzymology
Mice
Mice, Inbred C57BL
Mice, Knockout
Naphthalimides
/ pharmacology
CaMKK β
blood–brain barrier
hypoxia–ischemia
neonatal
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
26 Apr 2019
26 Apr 2019
Historique:
received:
29
03
2019
revised:
16
04
2019
accepted:
24
04
2019
entrez:
28
4
2019
pubmed:
28
4
2019
medline:
20
8
2019
Statut:
epublish
Résumé
Neonatal hypoxia-ischemia (HI) is a major cause of death and disability in neonates. HI leads to a dramatic rise in intracellular calcium levels, which was originally thought to be detrimental to the brain. However, it has been increasingly recognized that this calcium signaling may also play an important protective role after injury by triggering endogenous neuroprotective pathways. Calcium/calmodulin-dependent protein kinase kinase β (CaMKK β) is a major kinase activated by elevated levels of intracellular calcium. Here we evaluated the functional role of CaMKK β in neonatal mice after HI in both acute and chronic survival experiments. Postnatal day ten wild-type (WT) and CaMKK β knockout (KO) mouse male pups were subjected to unilateral carotid artery ligation, followed by 40 min of hypoxia (10% O
Identifiants
pubmed: 31027360
pii: ijms20092063
doi: 10.3390/ijms20092063
pmc: PMC6539688
pii:
doi:
Substances chimiques
Benzimidazoles
0
Naphthalimides
0
STO 609
0
Calcium-Calmodulin-Dependent Protein Kinase Kinase
EC 2.7.11.17
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Foundation for the National Institutes of Health
ID : NS099628
Références
Trends Biochem Sci. 1999 Jun;24(6):232-6
pubmed: 10366852
Stroke. 2001 Feb;32(2):570-6
pubmed: 11157199
Ann Neurol. 2004 Oct;56(4):468-77
pubmed: 15389899
Pediatr Neurol. 2004 Oct;31(4):254-7
pubmed: 15464636
J Neurosci. 2005 Oct 12;25(41):9544-53
pubmed: 16221865
Stroke. 2007 Oct;38(10):2826-32
pubmed: 17761909
Exp Hematol. 2008 Jul;36(7):832-44
pubmed: 18400360
Int J Obes (Lond). 2008 Sep;32 Suppl 4:S55-9
pubmed: 18719600
Behav Brain Res. 2009 Jan 30;197(1):77-83
pubmed: 18761039
Neuron. 2008 Sep 25;59(6):914-31
pubmed: 18817731
Mol Endocrinol. 2008 Dec;22(12):2759-65
pubmed: 18845671
Prog Neurobiol. 2009 Apr;87(4):264-80
pubmed: 19428957
Brain Res. 2009 Jul 14;1280:158-65
pubmed: 19450568
Physiol Rev. 2009 Jul;89(3):1025-78
pubmed: 19584320
Antioxid Redox Signal. 2011 Apr 1;14(7):1275-88
pubmed: 20615073
FEBS J. 2010 Sep;277(18):3622-36
pubmed: 20659161
J Neurosci Res. 2010 Nov 1;88(14):3144-54
pubmed: 20799369
Neuron. 2011 Jan 13;69(1):106-19
pubmed: 21220102
N Engl J Med. 2012 May 31;366(22):2085-92
pubmed: 22646631
Stroke. 2013 Sep;44(9):2559-66
pubmed: 23868268
BMC Neurosci. 2014 Oct 21;15:118
pubmed: 25331941
J Neurochem. 2015 Apr;133(2):242-52
pubmed: 25598140
J Neuroinflammation. 2015 Feb 20;12:32
pubmed: 25889641
Neuropharmacology. 2015 Dec;99:38-50
pubmed: 26187393
Neurobiol Dis. 2016 Jul;91:182-93
pubmed: 26969532
BMC Anesthesiol. 2017 Dec 08;17(1):168
pubmed: 29216818
Cell Transplant. 2018 Sep;27(9):1328-1339
pubmed: 29692197
Eur J Neurosci. 2019 Jan;49(1):27-39
pubmed: 30422362
Ann Neurol. 1981 Feb;9(2):131-41
pubmed: 7235629