Document Detail


Bcl-x(l) Bax interaction after transient global ischemia.
MedLine Citation:
PMID:  9701349     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Five minutes of bilateral common carotid artery occlusion in the Mongolian gerbil results in a selective, delayed death of CA1 pyramidal neurons. Although Bcl-2 appears to protect a variety of cells from cell death, the precise role of this apoptosis-regulating protein is complicated. We used immunoblots to estimate levels of Bcl-2, Bcl-x(l), and Bax at various times after carotid occlusion. Rather than Bcl-2, Bcl-x(l) appears to be the predominant neuroprotective form of this family of proto-oncogenes in the gerbil hippocampus. After transient ischemia, Bcl-2 and Bcl-x(l) protein levels remained the same. However, Bax levels were dramatically increased at 6 hours after ischemia, compared with sham-operated animals, and were still elevated at 72 hours after ischemia. To monitor dimerization interactions among theses apoptosis-regulating molecules, immunoprecipitation studies were conducted. These studies demonstrated that Bcl-x(l) association with Bax increases after ischemia. Therefore, Bax may disrupt the more favorable Bcl-x(l) (Bcl-2) interactions necessary for normal neuronal functioning and thus promote transient ischemic death.
Authors:
F J Antonawich; S Krajewski; J C Reed; J N Davis
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism     Volume:  18     ISSN:  0271-678X     ISO Abbreviation:  J. Cereb. Blood Flow Metab.     Publication Date:  1998 Aug 
Date Detail:
Created Date:  1998-08-21     Completed Date:  1998-08-21     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8112566     Medline TA:  J Cereb Blood Flow Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  882-6     Citation Subset:  IM    
Affiliation:
Department of Neurology and Program in Neurobiology, State University of New York at Stony Brook, 11794-8121, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Gerbillinae
Hippocampus / metabolism*,  pathology*
Ischemic Attack, Transient / metabolism*,  pathology
Male
Mice
Mice, Inbred C57BL
Neuroprotective Agents
Proto-Oncogene Proteins / metabolism*
Proto-Oncogene Proteins c-bcl-2 / metabolism*
Time Factors
bcl-2-Associated X Protein
bcl-X Protein
Grant Support
ID/Acronym/Agency:
NS 30559/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Bax protein, mouse; 0/Bcl2l1 protein, mouse; 0/Neuroprotective Agents; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein; 0/bcl-X Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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