Document Detail

Expression of c-jun, hsp72 and gfap following repeated unilateral common carotid artery occlusion in gerbils-correlates of delayed ischemic injury.
MedLine Citation:
PMID:  9666068     Owner:  NLM     Status:  MEDLINE    
The relationship between gene responses and cumulative ischemic damage, as induced by two 10 min episodes of unilateral common carotid artery (CCA) occlusion separated by 5 h, was examined by in situ hybridization histochemistry and terminal transferase biotinylated-dUTP nick end labeling (TUNEL) in the gerbil brain. Intense cell death was noticed starting from 5 h after the second ischemic insult, reaching maximum levels in the nucleus caudate-putamen and thalamus at 12-24 h, but in the cortex and hippocampus at 2 days post-ischemia. Although tissue damage developed gradually, the region of progressive infarction could be delineated as an area deficient in gfap mRNA starting from 12 h, more apparent 24 h after repeated ischemic insults. Hsp72 mRNA was strongly increased in the cortex, caudate-putamen, ventrolateral thalamus, CA1-CA4 fields and dentate gyrus in the early stages, i.e., 15 min-5 h post-ischemia. C-jun mRNA was also elevated in these structures except for the CA1 field, where mRNA levels remained low. In the caudate-putamen and thalamus, where DNA fragmentation occurred rapidly, c-jun and hsp72 mRNAs declined to almost basal levels within 12 h after repeated ischemia, whereas in the other structures, c-jun and hsp72 mRNAs decreased in a more delayed fashion by 24-48 h. The close association between the c-jun and hsp72 mRNA decline and the onset of injury may reflect a more general disruption of the transcription process probably as the consequence of secondary metabolic deterioration. The dissociation between c-jun and hsp72 mRNA expression in the CA1 field may indicate severe ischemic injury, surpassing the range of tissue salvage.
D M Hermann; T Kuroiwa; U Ito; G Mies
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Brain research     Volume:  799     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  1998 Jul 
Date Detail:
Created Date:  1998-09-11     Completed Date:  1998-09-11     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  35-43     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Elsevier Science B.V. All rights reserved.
Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Gleueler Str. 50, D-50931 Cologne, Germany.
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MeSH Terms
Arterial Occlusive Diseases / genetics*
Carotid Artery Diseases / genetics*
Carotid Artery, Common
DNA Fragmentation / genetics
Gene Expression* / genetics
Genes, jun*
Genetic Techniques
Glial Fibrillary Acidic Protein / genetics*
HSP72 Heat-Shock Proteins
Heat-Shock Proteins / genetics*
In Situ Hybridization
Ischemic Attack, Transient / genetics
RNA, Messenger / metabolism
Reg. No./Substance:
0/Glial Fibrillary Acidic Protein; 0/HSP72 Heat-Shock Proteins; 0/Heat-Shock Proteins; 0/RNA, Messenger

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