Document Detail


Tumor necrosis factor-like weak inducer of apoptosis and fibroblast growth factor-inducible 14 mediate cerebral ischemia-induced poly(ADP-ribose) polymerase-1 activation and neuronal death.
MedLine Citation:
PMID:  20955770     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor Fibroblast growth factor-inducible 14 (Fn14) are expressed in neurons. Here we demonstrate that TWEAK induces a dose-dependent increase in neuronal death and that this effect is independent of tumor necrosis factor alpha (TNF-α) and mediated by nuclear factor-kappa B (NF-κB) pathway activation. Incubation with TWEAK induces apoptotic cell death in wild-type (Wt) but not in Fn14 deficient (Fn14(-/-)) neurons. Intracerebral injection of TWEAK induces accumulation of poly(ADP-ribose) polymers (PAR) in Wt but not in Fn14(-/-) mice. Exposure to oxygen-glucose deprivation (OGD) conditions increases TWEAK and Fn14 mRNA expression in Wt neurons, and decreases cell survival in Wt but not in Fn14(-/-) or TWEAK deficient (TWEAK(-/-)) neurons. Experimental middle cerebral artery occlusion (MCAO) increases the expression of TWEAK and Fn14 mRNA and active caspase-3, and the cleavage of poly(ADP-ribose) polymerase-1 (PARP-1) with accumulation of PAR in the ischemic area in Wt but not Fn14(-/-) mice. Together, these results suggest a model where in response to hypoxia/ischemia the interaction between TWEAK and Fn14 in neurons induces PARP-1 activation with accumulation of PAR polymers and cell death via NF-κB pathway activation. This is a novel pathway for hypoxia/ischemia-induced TWEAK-mediated cell death and a potential therapeutic target for ischemic stroke.
Authors:
W B Haile; R Echeverry; F Wu; J Guzman; J An; J Wu; M Yepes
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-16
Journal Detail:
Title:  Neuroscience     Volume:  171     ISSN:  1873-7544     ISO Abbreviation:  Neuroscience     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-24     Completed Date:  2011-03-10     Revised Date:  2012-01-10    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1256-64     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
Affiliation:
Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / pathology
Cell Death / drug effects,  genetics
Cells, Cultured
Cerebral Cortex / cytology
Disease Models, Animal
Dose-Response Relationship, Drug
Embryo, Mammalian
Gene Expression Regulation / drug effects,  genetics
Glucose / deficiency
Hydrogen Peroxide / pharmacology
Infarction, Middle Cerebral Artery / enzymology*,  pathology*,  physiopathology
Mice
Mice, Knockout
Neurons / drug effects,  physiology*
Oxidants / pharmacology
Poly(ADP-ribose) Polymerases / metabolism*
Receptors, Tumor Necrosis Factor / deficiency,  metabolism
Signal Transduction / drug effects,  genetics
Tumor Necrosis Factor-alpha / pharmacology
Tumor Necrosis Factors / deficiency,  pharmacology
Grant Support
ID/Acronym/Agency:
HL-095063/HL/NHLBI NIH HHS; NS-062073/NS/NINDS NIH HHS; R01 NS062073-01A2/NS/NINDS NIH HHS; R01 NS062073-04/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Oxidants; 0/Receptors, Tumor Necrosis Factor; 0/TWEAK receptor; 0/Tnfsf12 protein, mouse; 0/Tumor Necrosis Factor-alpha; 0/Tumor Necrosis Factors; 50-99-7/Glucose; 7722-84-1/Hydrogen Peroxide; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 2.4.2.30/poly(ADP-ribose)polymerase-1, mouse

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