Project/Area Number |
15KT0009
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Multi-year Fund |
Section | 特設分野 |
Research Field |
Neo-Gerontology
|
Research Institution | Keio University |
Principal Investigator |
ARAI YASUMICHI 慶應義塾大学, 医学部(信濃町), 講師 (20255467)
|
Co-Investigator(Kenkyū-buntansha) |
石崎 達郎 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究部長 (30246045)
権藤 恭之 大阪大学, 人間科学研究科, 准教授 (40250196)
神出 計 大阪大学, 医学系研究科, 教授 (80393239)
湯浅 慎介 慶應義塾大学, 医学部(信濃町), 講師 (90398628)
中岡 博史 国立遺伝学研究所, 総合遺伝研究系, 助教 (70611193)
|
Co-Investigator(Renkei-kenkyūsha) |
IKEBE Kazunori 大阪大学, 医学系研究科, 教授 (70273696)
INOUE Itsurou 国立遺伝学研究所, 人類遺伝研究部門, 教授 (00192500)
|
Project Period (FY) |
2015-07-10 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2017: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2016: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
|
Keywords | 超百寿者 / iPS細胞 / 健康長寿 / 疫学 / 血管内皮 / 異分野連携 / 百寿者 / ストレス耐性 / iPS / 低酸素応答 / 動脈硬化 / コホート研究 / 遺伝多型 |
Outline of Final Research Achievements |
In this project, we aimed to identify key molecules of stress resistance in supercentenarians by means of induced pluripotent stem (iPS) cells, and replicate the findings in a cohort study of older adults, the SONIC study. First, we established iPS cells-derived endothelial cells from supercentenarians, and examined key molecules of oxidative stress and hypoxic stress responses. However, transcriptional study failed to identify key molecules because of small sample size. Alternatively, we performed QTL analysis for extracellular-superoxide dismutase (EC-SOD), a circulating antioxidative stress molecule, and identified SNP in rs1799895 as significant determinant for circulating EC-SOD. We genotyped this SNP in 1,890 subjects in the SONIC study, and found significant associations between the SNP and carotid atherosclerosis, and geriatric phenotype.
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