Expression of insulin-like growth factor-binding protein 2 (IGF-BP 2) following transient hypoxia-ischemia in the infant rat brain
| Autor: | Peter D. Gluckman, M. Klempt, N.D. Klempt, Kuljeet Singh, Alistair J. Gunn |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
medicine.medical_specialty
Central nervous system Ischemia Hippocampus In situ hybridization Insulin-like growth factor-binding protein Cellular and Molecular Neuroscience Oxygen Consumption Internal medicine medicine Animals Rats Wistar Hypoxia Molecular Biology In Situ Hybridization biology Hypoxia (medical) medicine.disease Blotting Northern Rats Insulin-Like Growth Factor Binding Protein 2 medicine.anatomical_structure Endocrinology nervous system Animals Newborn Ischemic Attack Transient Insulin-like growth factor 2 biology.protein Choroid plexus medicine.symptom Carrier Proteins Neuroscience |
| Zdroj: | Brain research. Molecular brain research. 15(1-2) |
| ISSN: | 0169-328X |
| Popis: | Hypoxia-ischemia induced by unilateral carotid ligation followed by either 15 (moderate) or 90 (severe) min exposure to 8% oxygen was associated with induction of IGF-BP 2 mRNA expression. A specific rat IGF-BP 2 cDNA probe was used to determine the IGF-BP 2 mRNA distribution in brain sections using in situ hybridization. Untreated control rats and the non-ligated hemisphere in experimental rats expressed IGF-BP 2 mRNA in the choroid plexus, meninges and more weakly in the thalamus, hippocampus and cortical layer 5. Increased expression in experimental rats was limited to regions known to have neuronal damage. Three days after the moderate insult the signal was increased in the CA1/2 region of the hippocampus and thalamus of the ligated side. Three days after the severe insult IGF-BP 2 expression was found surrounding the infarcted regions while by 5 days after severe insult the whole infarcted volume showed induction. The results suggest a role for the IGFs in the post-asphyxial response. IGF-BP 2 may alter the bio-availability of IGF 1 or 2 or modulate their actions in the area of infarction, and thus promote cerebral repair and recovery. |
| Databáze: | OpenAIRE |
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