| Project/Area Number |
15K10286
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurosurgery
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| Research Institution | Hokkaido University |
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Principal Investigator |
KAZUMATA Ken 北海道大学, 大学病院, 講師 (60634144)
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| Co-Investigator(Kenkyū-buntansha) |
中山 若樹 北海道大学, 医学研究院, 講師 (40421961)
鐙谷 武雄 北海道大学, 大学病院, 助教 (80270726)
七戸 秀夫 北海道大学, 大学病院, 准教授 (80374479)
寳金 清博 北海道大学, 大学病院, 教授 (90229146)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | もやもや病 / iPS細胞 / 血管内皮細胞 / 内皮細胞 / バリア機能 / tight junction |
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| Outline of Final Research Achievements |
We differentiated vascular endothelial cells from iPS cells derived from healthy persons and moyamoya disease patients. The expression of cell junction related genes were analysed with microarray and the result showed that CLDN1, DST, NEXN and ITGB3 were down-regulated in moyamoya disease. RT-PCR showed that ITGB3 was significantly downregulated in moyamoya disease, however, there were no significat difference in the expression of DST and NEXN. We could not observe the band intensity of CLDN1 in neither RT-PCR and western blotting. In permeability assay, permeability was increased in endothelial cells of moyamoya disease when Y-27632 was added to medium, whereas permeability decreased in normal control.
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