| Project/Area Number |
21790721
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
SONE Masakatsu Kyoto University, 医学研究科, 助教 (40437207)
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| Research Collaborator |
TAURA Daisuke , 日本学術振興会特別研究員(PD)
HOMMA Koichiro 京都大学, 医学研究科, 客員研究員
SUZUKI Yutaka NPO法人幹細胞創薬研究所
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 血管 / 再生 / ES / iPS / 分化 / 老化 / 分子血管病怠学 / 内分泌学 / 循環器病学 / iPS細胞 / 抗加齢医学 |
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| Research Abstract |
We succeeded in inducing iPS cells to differentiate into vascular endothelial cells (ECs) and mural cells (MCs), which we were able to isolate. We also established a feeder- and serum-free method that enables us to more efficiently induce ECs. Human ES-derived ECs (ESECs) and iPS-derived ECs (iPSECs) had a greater potential for wound re-endothelialization and tube formation than human adult ECs (HAECs) in vitro. Next we carried out a gene expression analysis of these three types of ECs using gene chip technology. The expression level of Sirt1, an aging-related gene that encodes a NAD-dependent histone deacetylase, was higher in ESECs/iPSECs than in HAECs. When Sirt1 activity was knocked down by siRNA or inhibited by a specific Sirt1 antagonist, the aforementioned differences in the cellular functionality were abolished, which suggests that differences in Sirt1 activity contribute to the observed differences in the cellular functionality.
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