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- W2065832420 abstract "The precise molecular mechanism of ischemic stroke is still unclear. We examined the detailed role of hypoxia-inducible factor-1-alpha (HIF-1α) in experimental stroke. We examined the role of HIF-1α in ischemic brain by using immunoprecipitation, Western blotting and behavior test. We also examined the efficacy of echinomycin (HIF-1α inhibitor) on ischemic stroke In the present study, biphasic expression of HIF-1α in neurons exposed to ischemic stress in vitro and in vivo was observed. In addition to hypoxia, excessive glutamate was also involved in early phase HIF-1α expression through activation of the N-methyl-D-aspartate (NMDA) receptor. Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) were both necessary to late rather than early phase HIF-1α expression. Specific inhibition of early phase HIF-1α by echinomycin decreased brain injury and downregulated Nix expression. Conversely, late phase expression of HIF-1α played a protective role. Treating neurons with echinomycin 24 hours after ischemic stress increased neuron damage and decreased vascular endothelial growth factor (VEGF) expression. Finally, p53, but not ARNT1 or p300, was specifically associated with first phase HIF-1α, which could be blocked by an NMDA receptor antagonist. These results demonstrate new insight into the opposing roles of HIF-1α expression in neurons after ischemic stroke. Conclusion - We obtained the evidence that the bipoasic expression of HIF-1 played either Pro-death or pro-survival effect in rat model of transient focal cerebral ischemia." @default.
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- W2065832420 date "2009-07-01" @default.
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- W2065832420 title "P4-220: Divergent effects of HIF-1α in rat model of transient focal cerebral ischemia" @default.
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