Project/Area Number |
15K08238
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | University of the Ryukyus |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
筒井 正人 琉球大学, 医学(系)研究科(研究院), 教授 (70309962)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 一酸化窒素 / 血管内皮細胞機能 / ジヒドロビオプテリン / テトラヒドロビオプテリン / ジヒドロ葉酸還元酵素 / 酸化ストレス / 血管内皮細胞 / 血管内皮機能 / dihydrofolate reductase / 遺伝子導入マウス |
Outline of Final Research Achievements |
An elevation of oxidized forms of tetrahydrobiopterin (BH4), especially dihydrobiopterin (BH2), has been reported in the setting of oxidative stress, such as atherosclerotic disorders, where eNOS is dysfunctional, but a role of dihydrofolate reductase (DHFR), an enzyme catalyzing intracellular conversion of BH2 to BH4, in the regulation of endothelial function in vivo remains to be clarified. To this end, we generated novel mice with endothelium-specific deficiency of Dhfr gene, endothelium-specific and temporal deficiency of the gene and with endothelium-specific expression of DHFR transgene, and we examined characteristics of phenotypes of these mice.
|