| Project/Area Number |
24792237
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Surgical dentistry
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| Research Institution | Kumamoto University |
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Principal Investigator |
TAMURA Kiyomi 熊本大学, 発生医学研究所, 助教 (90399973)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 血管 / Foxo1 / 胚性幹細胞（ES細胞） / 転写因子 / 胚性幹細胞 |
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| Research Abstract |
Transcription factor Forkhead box O1 (Foxo1) (-/-) mice fail to develop vascular structure and are embryonic lethal by E11. So, Foxo1 is essential for the vascular development. However the mechanism is unclear.
In vitro vessel-like structure formation of ES cells are the useful examination system for vascular formation. In this model, vascular endothelial cells (ECs) derived from wild type ES cells showed the long and thin elongated morphology, but Foxo1 (-/-) EC failed to elongate. And, wild type pericytes can associate with wild type EC. Foxo1 (-/-) cells show no-association between EC and pericytes. To identify the Foxo1 target genes that are responsible for the regulation of EC elongation, I analyzed gene expression profiles of ECs and rescue studies of putative target genes. As a result, I identified an putative target gene. Furthermore, analysis of EC specific Foxo1 expressing ES cells show that Foxo1 in EC regulates EC-pericyte association.
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