Document Detail


Delayed IGF-1 administration rescues oligodendrocyte progenitors from glutamate-induced cell death and hypoxic-ischemic brain damage.
MedLine Citation:
PMID:  17762198     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We previously demonstrated that IGF-1 blocks glutamate-mediated death of late oligodendrocyte progenitors (OPs) by preventing Bax translocation, mitochondrial cytochrome c release and cleavage of caspases 9 and 3. Here, we demonstrate that IGF-1 prevents caspase 3 activation in late OPs when administered up to 16 h following exposure to glutamate. Moreover, late addition of IGF-1 to OPs previously exposed to toxic levels of glutamate promotes oligodendrocyte maturation as measured by myelin basic protein expression. We also demonstrate that intraventricularly administered IGF-1 retains OPs in the perinatal white matter after hypoxia-ischemia when given after insult. These results suggest that delayed administration of IGF-1 will rescue OPs in the immature white matter and promote myelination following hypoxia-ischemia.
Authors:
Teresa L Wood; Vaho Loladze; Stefanie Altieri; Nitish Gangoli; Steven W Levison; Katarina G Brywe; Carina Mallard; Henrik Hagberg
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Developmental neuroscience     Volume:  29     ISSN:  1421-9859     ISO Abbreviation:  Dev. Neurosci.     Publication Date:  2007  
Date Detail:
Created Date:  2007-08-31     Completed Date:  2007-10-05     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  7809375     Medline TA:  Dev Neurosci     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  302-10     Citation Subset:  IM    
Copyright Information:
2007 S. Karger AG, Basel
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Apoptosis / drug effects*,  physiology
Caspase 3 / drug effects,  metabolism
Cells, Cultured
Cytoprotection / drug effects,  physiology
Drug Administration Schedule
Glutamic Acid / toxicity
Hypoxia-Ischemia, Brain / drug therapy*,  metabolism,  physiopathology
Insulin-Like Growth Factor I / pharmacology*
Myelin Basic Protein / metabolism
Nerve Degeneration / drug therapy*,  physiopathology,  prevention & control
Nerve Fibers, Myelinated / drug effects,  metabolism
Nerve Growth Factors / pharmacology
Neurotoxins / toxicity
Oligodendroglia / drug effects*,  metabolism
Rats
Rats, Sprague-Dawley
Rats, Wistar
Stem Cells / drug effects*,  metabolism
Time Factors
Treatment Outcome
Grant Support
ID/Acronym/Agency:
NS37560/NS/NINDS NIH HHS; NS50742/NS/NINDS NIH HHS; R01 MH059950/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Myelin Basic Protein; 0/Nerve Growth Factors; 0/Neurotoxins; 3KX376GY7L/Glutamic Acid; 67763-96-6/Insulin-Like Growth Factor I; EC 3.4.22.-/Caspase 3

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


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