HYPOXIA-INDUCED VASCULAR ENDOTHELIAL GROWTH FACTOR EXPRESSION PRECEDES NEOVASCULARIZATION AFTER CEREBRAL ISCHEMIA

摘要: We investigated the hypothesis that hypoxia induces angiogenesis and thereby may counteract detrimental neurological effects associated with stroke. Forty-eight to seventy-two hours after permanent middle cerebral artery occlusion we found a strong increase in number of newly formed vessels at border infarction. Using marker nitroimidazole EF5, detected hypoxic cells ischemic neocortex. Expression vascular endothelial growth factor (VEGF), which is main regulator inducible by hypoxia, was strongly up-regulated border, times between 6 24 occlusion. In addition, both VEGF receptors (VEGFRs) were 48 later core. Finally, two transcription factors, hypoxia-inducible factor-1 (HIF-1) HIF-2, known be involved regulation VEGFR gene expression, increased 72 hours, suggesting regulatory function for these factors. These results suggest VEGF/VEGFR system, induced leads new ischemia. Exogenous support this natural protective mechanism might lead enhanced survival