J Korean Neurol Assoc > Volume 20(6); 2002 > Article

Journal of the Korean Neurological Association 2002;20(6): 634-640.

"시험관 내 허혈 환경에서 혈관내피 성장인자의 발현과 신경보호효과"

한문구, 김만호 나정호 이용석 김승업노재규

"을지대학교 의과대학 신경과학교실＊,인하대학교 의과대학 신경과학교실, 아주대학교 의과대학 신경과학교실,서울대학교 의과대학교 신경과학교실"

"Expression and Neuroprotection of Vascular Endothelial Growth Factor in an in vitro Ischemia"

Moon-Ku Han

"Department of Neurology, Eulji University School of Medicine, Inha University School of Medicine ,Ajou University School of Medicine ,Seoul University School of Medicine"

Abstract

"Background : Vascular endothelial growth factor (VEGF) is an angiogenic peptide that enhances microvascular per-fusion. Recently, VEGF is known to have neurotrophic effect and rescues neurons from cell death induced by serum deprivation. To investigate the serial changes in VEGF expression and neuroprotective properties of VEGF during acute ischemia. Methods : Human cortical-neuroblastoma hybrid cell line (A1G11), human neuroglioma cell line (H4), and human vascular endothelial cell line (ECV304) were placed in the glucose/serum free media and incubated in the hypoxic chamber (94% N2/5% CO2/1% room air) at 37 ℃. Cell viability was determined by MTT assay. Western blot analysis was performed to detect VEGF and its receptor (VEGFR) expression. To test the protective effect of VEGF, human recombinant VEGF165 was used.
Results: Morphological changes and the decrease of cell viability were observed following 6 hr ischemia. In A1G11 cells, VEGF expression was not noted until 3 hr ischemia, but was induced after 6hr and continued to 12 hr and then diminished. In H4 and ECV304, the change of VEGF expression was not observed. VEGFR-2/Flk-1 expression was induced from 6 hr (peak level) to 12 hr in A1G11, and induced after 3 hr and continued to 12hr in ECV304. Administration of VEGF increased cell viability in A1G11 cells at 6 hr, 12 hr and 18 hr ischemia (p=0.009, p=0.01 p=0.013), but not in H4 or ECV304 cells ( p > 0.05). Conclusion : Ischemia induces VEGF production in neurons and VEGF may exert a direct neuron-specific protective effect through VEGFR-2/Flk receptors during the acute phase of ischemic neuronal injury."