Does Runx1 produce hematopoietic stem cell from hemogenic endothelium via Endothelial to Mesenchymal Transition?
| Project/Area Number |
23590345
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
YAMAMOTO Yasutoshi 京都府立医科大学, 医学(系)研究科(研究院), 助教 (50405247)
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| Co-Investigator(Kenkyū-buntansha) |
OKUDA Tsukasa 京都府立医科大学, 医学(系)研究科(研究院), 教授 (30291587)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 血球産生型血管内皮 / 造血幹細胞 / Runx1 |
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| Research Abstract |
The aim of this study is to investigate the molecular mechanism in the process of hematopoietic stem cells (HSCs) emergence from the hemogenic endothelium by the hematopoietic transcription factor AML1/Runx1. We originally succeeded in the production of knock in mouse which had reporter gene (GFP) targeting the Runx1 locus and could observe GFP signal in this mouse. We also discovered Runx1 depending factor, endothelial mesenchymal transition related transcription factor, by using comprehensive gene expression analysis against embryonic stem cell differentiation model. Runx1 gene knock down effects on the downregulation of this transcriptional factor and upregulation of the tight junction which dissolves at the HSCs emergence. These findings suggest that Runx1 can transform vascular endothelium with polarity and tight adhesion into HSCs via hemogenic endothelium.
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Report
(4 results)
Research Products
(12 results)
