期刊
DEVELOPMENTAL NEUROSCIENCE
卷 29, 期 4-5, 页码 302-310出版社
KARGER
DOI: 10.1159/000105471
关键词
insulin-like growth factor; trophic factors; periventricular leukomalacia; white matter damage; excitotoxicity; apoptosis; myelin
资金
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH059950] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS050742, R01NS037560] Funding Source: NIH RePORTER
- NIMH NIH HHS [R01 MH059950] Funding Source: Medline
- NINDS NIH HHS [NS37560, NS50742] Funding Source: Medline
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. Copyright c 2007 S. Karger AG, Basel.
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