Project/Area Number |
24591260
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurology
|
Research Institution | Osaka University |
Principal Investigator |
YAGITA Yoshiki 大阪大学, 医学(系)研究科(研究院), 招へい教員 (20403066)
|
Co-Investigator(Kenkyū-buntansha) |
KITAGAWA Kazuo 東京女子医科大学, 医学部, 教授 (70301257)
OYAMA Naoki 大阪大学, 医学部付属病院, その他 (90622895)
|
Co-Investigator(Renkei-kenkyūsha) |
MOCHIZUKI Hideki 大阪大学, 医学系研究科, 教授 (90230044)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | 脳小血管 / 血管内皮 / 脳虚血 / 細胞接着 / 血管内皮細胞 / 血液脳関門 |
Outline of Final Research Achievements |
VE-cadherin mediated endothelial cell-cell junction play an important role to form barrier in the brain. VEGF was induced after ischemia and might suppress the VE-cadherin mediated cell-cell adhesion via increasing in interaction with IQGAP1. TNFα is another molecule to induce vascular permeability in diabetes mellitus. We found TNFα was increased in the brain parenchyma in db/db mice. eNOS is one of key molecule to maintain the endothelial function. In the ischemic brain, eNOS monomer was increased and nitrotyrosine signals were observed in the cerebral endothelial cells. These results may contribute to develop new therapy for acute ischemia and small vessel disease in the brain.
|