2011 Fiscal Year Final Research Report
Mechanism of endothelial dysfunction in the acute brain ischemia and development of therapeutic intervention.
| Project/Area Number |
21591080
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Osaka University |
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Principal Investigator |
YAGITA Yoshiki 大阪大学, 医学系・研究科, 助教 (20403066)
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| Co-Investigator(Kenkyū-buntansha) |
KITAGAWA Kazuo 大阪大学, 医学系・研究科, 准教授 (70301257)
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| Research Collaborator |
SAKODA Saburo 刀根山病院, 院長
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| Project Period (FY) |
2009 – 2011
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| Keywords | 脳虚血 / 血管内皮 / 微小循環障害 / Rho-kinase / 一酸化窒素合成酵素 |
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| Research Abstract |
Endothelial nitric oxide synthase(eNOS) is one of key molecules to maintain endothelial function. Although eNOS expression was increased in the brain small vessels after cerebral ischemia, phosphorylation level of Ser1177 of eNOS molecule was significantly reduced, indicating eNOS dysfunction. Rho-kinase inhibitor can ameliorate ischemic injury via increasing eNOS phosphorylation. Hypertension also decreased eNOS phosphorylation in the brain small vessels and deteriorated ischemic injury, and anti-hypertensive therapy could preserve eNOS phosphorylation. Additionally, phosphodiesterase3 could preserve eNOS phosphoryaltion and function and ameliorated cerebral ischemic injury. These results may contribute to develop new therapy for acute brain ischemia and brain small vessel disease.
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