Elucidation of mechanism of increase in oxidative stress related to intrinsic susceptibility in brain microvascular endothelial cells

Research Project

Project/Area Number	20591681
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Cerebral neurosurgery
Research Institution	Hokkaido University
Principal Investigator	ABUMIYA Takeo Hokkaido University, 大学院・医学研究科, 非常勤講師 (80270726)
Co-Investigator(Kenkyū-buntansha)	IWASAKI Yoshinobu 北海道大学, 名誉教授 (00113522) HIDA Kazutoshi 北海道大学, 大学院・医学研究科, 准教授 (10238305) KURODA Satoshi 北海道大学, 病院, 講師 (10301904)
Project Period (FY)	2008 – 2010
Project Status	Completed (Fiscal Year 2010)
Budget Amount *help	¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000) Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2008: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Keywords	脳微小血管 / 血管内皮細胞 / 酸化ストレス / 活性酸素
Research Abstract	We investigated intrinsic susceptibility and its associated increase of oxidative stress in brain microvascular endothelial cells (BMEC) by comparing BMEC and aortic endothelial cells (AEC). When investigating the effect of advanced glycation end products on molecular permeability, the molecular permeability was more prominent in BMEC than in AEC. The susceptibility in BMEC was dependent on VEGF expression induced by over-production of reactive oxygen species. When investigating the effect of hyperglycemia on production of reactive oxygen species in BMEC and AEC, the production was increased in hyperglycemia. Since NOX4, one of subunits of NADPH oxidases, was also increased in the same hyperglycemic condition, we speculate that NOX4 is related to hyperglycemia-induced over-production of reactive oxygen species.