Hypoxia and hypoxia/ischemia affect the expression of insulin-like growth factor binding protein 2 in the developing...

Brain halves were collected at various time points from 21-day-old Wistar rats exposed to either a short or prolonged period of inhalational hypoxia following unilateral carotid ligation post-insult. Neuronal loss was restricted to the side of the carotid ligation. Northern blot analysis was performed for IGFBP-2 mRNA. The prolonged hypoxia decreased the expression of IGFBP-2 five hours post insult, whereas the shorter insult level showed an (P < 0.05) increase above control. In both groups IGFBP-2 mRNA increased to peak 3-5 days post insult. After a decline at day 6, expression was again high 7-10 days after HI. In the short hypoxia group, where there was little neuronal loss, the expression of IGFBP-2 in both hemispheres followed the same pattern over time. However prolonged hypoxia induced higher IGFBP-2 expression in the ligated hemisphere where there was extensive neuronal loss. At day 5 post-insult 5/9 rats showed an additional, slightly smaller (1.4 kb vs 1.7 kb) second transcript. The different pattern of expression associated with different degrees of injury suggest that IGFBP-2 is involved in the post asphyxial response. Hypoxia itself leads to alterations in IGFBP-2 expression. Greater expression is associated with neuronal loss. These observations suggest that the IGF system contributes to neuronal rescue and/or brain repair processes.