| E-selectin Mrna and Protein Expression Increase Transiently After Unilateral Cerebral hypoxia-ischemia in Neonatal Rats. |
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Baik Lin Eun |
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| Abstract |
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BACKGROUND AND PURPOSE: The selectins play a role in the initiation of endothelium-leukocyte interaction; endothelial expression of E-selectin is induced by ischemia-reperfusion-like conditions in vitro. Neutrophils accumulate in post-hypoxic-ischemic neonatal rat brain prior to the evolution of necrosis and neutrophil depletion attenuates hypoxic-ischemic brain injury; the mechanisms leading to post-hypoxic-ischemic neutrophil accumulation are unknown. We hypothesized that E-selectin might mediate post-hypoxic-ischemic injury in the immature brain, thus, we evaluated E- selectin gene expression by RT-PCR and protein accumulation by immunocytochemistry in post-hypoxic-ischemic neonatal (postnatal day 7) rat brain. METHODS: Neonatal rats (n=48) underwent right carotid ligation followed by 2h in 8% O2; this procedure typically produces ipsilateral striatal, hippocampal and cortical infarction. Controls included carotid ligation alone, hypoxia alone, and neither hypoxia nor ligation. For RNA extraction, rats were killed 0, 1, 2, 4, 8, 12, 24 and 48 h post-hypoxia-ischemia. For immunocytochemistry, rats were killed at 4 and 8 h. RESULTS: Ipsilateral(right-sided) E-selectin mRNA was markedly elevated in cortex, striatum and hippocampus at 4 and 8 h post-hypoxia-ischemia; expression decreased at 12 and 24 h and was no longer detectable at 48 h. E-selectin protein was detected predominantly in right striatum 8 h post-hypoxia-ischemia, in a pattern consistent with a vascular distribution. E-selectin mRNA was barely detectable in any controls. CONCLUSION: The temporal and spatial profiles of post-hypoxic-ischemic E-selectin mRNA and protein expression are consistent with a role in post-hypoxic-ischemic neutrophil recruitment and in the evolution of subsequent brain injury. |
| Key Words:
E-selectin, Cerebral hypoxia-ischemia, Neonatal, Perinatal |
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