Document Detail


Influence of duration of focal cerebral ischemia and neuronal nitric oxide synthase on translocation of apoptosis-inducing factor to the nucleus.
MedLine Citation:
PMID:  17049179     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus can play a major role in neuronal death elicited by oxidant stress. The time course of nuclear translocation of AIF after experimental stroke may vary with the severity of injury and may be accelerated by oxidant stress associated with reperfusion and nitric oxide (NO) production. Western immunoblots of AIF on nuclear fractions of ischemic hemisphere of male mice showed no significant increase with 1 h of middle cerebral artery occlusion and no reperfusion, whereas increases were detectable after 6 and 24 h of permanent ischemia. However, as little as 20 min of reperfusion after 1 h of middle cerebral artery occlusion resulted in an increase in nuclear AIF coincident with an increase in poly(ADP-ribose) polymer (PAR) formation. Further nuclear AIF accumulation was seen at 6 and 24 h of reperfusion. In contrast, 20 min of reperfusion after 2 h of occlusion did not increase nuclear AIF. In this case, nuclear AIF became detectable at 6 and 24 h of reperfusion. With brief occlusion of 30 min duration, nuclear AIF remained undetectable at both 20 min and 6 h and became evident only after 24 h of reperfusion. Inhibition of neuronal NO synthase attenuated formation of PAR and nuclear AIF accumulation. Gene deletion of neuronal NO synthase also attenuated nuclear AIF accumulation. Therefore, reperfusion accelerates AIF translocation to the nucleus when focal ischemia is of moderate duration (1 h), but is markedly delayed after brief ischemia (30 min). Nuclear translocation of AIF eventually occurs with prolonged focal ischemia with or without reperfusion. Neuronally-derived NO is a major factor contributing to nuclear AIF accumulation after stroke.
Authors:
X Li; M Nemoto; Z Xu; S-W Yu; M Shimoji; S A Andrabi; J-F Haince; G G Poirier; T M Dawson; V L Dawson; R C Koehler
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-10-13
Journal Detail:
Title:  Neuroscience     Volume:  144     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2007 Jan 
Date Detail:
Created Date:  2006-12-12     Completed Date:  2007-03-15     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  56-65     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, The Johns Hopkins University, 600 North Wolfe Street, Blalock 1404, Baltimore, MD 21287, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis Inducing Factor / metabolism*
Behavior, Animal / physiology
Blotting, Western
Cell Nucleus / metabolism*
Enzyme Inhibitors / pharmacology
Gene Deletion
Indazoles / pharmacology
Infarction, Middle Cerebral Artery / pathology,  psychology
Ischemic Attack, Transient / pathology*,  psychology
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Neurons / enzymology*
Nitric Oxide Synthase Type I / antagonists & inhibitors,  genetics,  metabolism*
Poly Adenosine Diphosphate Ribose / metabolism
Protein Transport
Reperfusion Injury / pathology,  psychology
Subcellular Fractions / metabolism
Time Factors
Grant Support
ID/Acronym/Agency:
P01 NS039148-080006/NS/NINDS NIH HHS; P01 NS39148/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Apoptosis Inducing Factor; 0/Enzyme Inhibitors; 0/Indazoles; 26656-46-2/Poly Adenosine Diphosphate Ribose; 2942-42-9/7-nitroindazole; EC 1.14.13.39/Nitric Oxide Synthase Type I
Comments/Corrections

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