Document Detail


Sequential activation of activator protein-1-related transcription factors and JNK protein kinases may contribute to apoptotic death induced by transient hypoxia in developing brain neurons.
MedLine Citation:
PMID:  9838068     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies have demonstrated that transient hypoxia (6 h) induces apoptotic death in cultured neurons isolated from the fetal rat forebrain. Since activation of c-Jun N-terminal kinases (JNKs) and subsequent phosphorylation of c-Jun are suspected to be involved in the apoptotic pathway in several cell types, the time course of activator protein-1 (AP-1) DNA-binding, in line with induction of the AP-1 components and JNK activation, was examined during hypoxia/reoxygenation in the same model. Gel shift analysis depicted the presence of functional AP-1 transcription factors in both control and hypoxic neurons. One hour after the onset of hypoxia, all AP-1 components were markedly overexpressed. They include c-Jun, Jun B, Jun D, c-Fos and Fos-related antigens. Whereas, only c-Jun remained elevated for up to 96 h post-reoxygenation, time at which neurons were injured, other gene products showed patterned induction/repression as hypoxia progressed and then during the post-reoxygenation period, with Fos-related antigens being finally induced at 96 h. Only JNK1 was constitutively detected in cultured neurons, and its expression was inhibited during hypoxia. Nonetheless, both JNK1 and JNK3 were markedly, but transiently, induced at 48 h post-reoxygenation, when apoptosis-related morphological features became apparent. These data support the hypothesis that transient hypoxia, independently of ischemia, may trigger apoptosis through JNK signaling pathway in developing brain neurons.
Authors:
R Chihab; C Ferry; V Koziel; P Monin; J L Daval
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Brain research. Molecular brain research     Volume:  63     ISSN:  0169-328X     ISO Abbreviation:  Brain Res. Mol. Brain Res.     Publication Date:  1998 Dec 
Date Detail:
Created Date:  1999-01-21     Completed Date:  1999-01-21     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8908640     Medline TA:  Brain Res Mol Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  105-20     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Elsevier Science B.V.
Affiliation:
JE 2164 and INSERM U.272, Université Henri Poincaré-Nancy 1, Nancy, France.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies
Apoptosis / physiology*
Brain / blood supply,  embryology,  enzymology
Brain Chemistry / physiology
Cell Survival / physiology
Cells, Cultured
Female
Hypoxia, Brain / physiopathology*
Ischemic Attack, Transient / physiopathology
JNK Mitogen-Activated Protein Kinases*
MAP Kinase Kinase 4
Male
Mitogen-Activated Protein Kinase Kinases*
Neurons / chemistry,  cytology*,  enzymology
Pregnancy
Protein Kinases / analysis,  immunology,  metabolism*
Rats
Rats, Sprague-Dawley
Reperfusion Injury / physiopathology
Transcription Factor AP-1 / analysis,  immunology,  metabolism*
Chemical
Reg. No./Substance:
0/Antibodies; 0/Transcription Factor AP-1; EC 2.7.-/Protein Kinases; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases; EC 2.7.12.2/MAP Kinase Kinase 4; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases

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


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