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Delayed IGF-1 admin...
Delayed IGF-1 administration rescues oligodendrocyte progenitors from glutamate-induced cell death and hypoxic-ischemic brain damage.
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Wood, Teresa L (författare)
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Loladze, Vaho (författare)
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Altieri, Stefanie (författare)
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Gangoli, Nitish (författare)
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Levison, Steven W (författare)
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- Gustafsson Brywe, Katarina, 1965 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Clinical Sciences,Institute of Neuroscience and Physiology, Department of Physiology
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- Mallard, Carina, 1963 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
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- Hagberg, Henrik, 1955 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institutionen för kliniska vetenskaper,Institute of Neuroscience and Physiology, Department of Physiology,Institute of Clinical Sciences
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(creator_code:org_t)
- 2007-08-31
- 2007
- Engelska.
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Ingår i: Developmental neuroscience. - : S. Karger AG. - 1421-9859 .- 0378-5866. ; 29:4-5, s. 302-10
- Relaterad länk:
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https://www.karger.c...
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https://gup.ub.gu.se...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- 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.
Nyckelord
- 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 Proteins
- 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
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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