Elucidation of the regulatory mechanism for claudin-5 expression in vascular endothelial cells
| Project/Area Number |
23590447
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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 |
Experimental pathology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
CUI Dan 山口大学, 医学(系)研究科(研究院), 講師 (40346549)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Eiji 山口大学, 大学院医学系研究科, 教授 (30232177)
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| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 血液脳関門 / 血液網膜関門 / タイト結合 / 低酸素 / クローディン５ / グローディン５ / タイト結結合 |
|---|
| Research Abstract |
Tissue hypoxia is known to accelerate the progression of intractable neural diseases through the breakdown of neural vascular barrier including the blood-brain barrier and the inner blood-retinal barrier. However, the mechanisms underlying the hypoxia-induced breakdown of vascular barrier remain unclarified. Here, using the in vitro and in vivo models of neural vascular barrier, we have specified two molecules, M1 and M2, as the indispensable molecules for hypoxia-induced breakdown of neural vascular barrier, and therefore the candidate molecules for new therapeutic targets of intractable neural diseases.
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Report
(4 results)
Research Products
(7 results)
