2018 Fiscal Year Final Research Report
Study of the regulation of hematopoietic stem cell self-renewal mediated by the control of actin polymerization
Project/Area Number |
16K09824
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Hematology
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Research Institution | Kanazawa University |
Principal Investigator |
TADOKORO Yuko 金沢大学, がん進展制御研究所, 助教 (00447343)
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | 幹細胞 / 自己複製 / アクチン |
Outline of Final Research Achievements |
Interactions between tissue-specific stem cells and their microenvironment known as niche play important roles in the stem cell fate determination such as the maintenance, proliferation, and differentiation. In this study, we aim to elucidate the regulatory mechanisms of hematopoietic stem cell self-renewal mediated by the control of actin polymerization. In particular, we focused on the roles of Spred1, which is a negative regulator of ROCK and ERK signaling pathways, in hematopoietic stem cell (HSC) function. We have clearly shown that the control of actin polymerization mediated by Spred1-ROCK signaling pathway regulates the self-renewal capacity of HSCs. Furthermore, we have elucidated that Spred1 prevents high fat diet-induced tumorigenesis of HSCs through the regulation of ERK signaling pathway.
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Free Research Field |
幹細胞生物学
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Academic Significance and Societal Importance of the Research Achievements |
偏った食習慣は様々な疾患の原因になると考えられているが、幹細胞がどのような影響を受けるかについてはあまり知られていない。本研究成果においては、アクチン重合調節が造血幹細胞の自己複製制御に重要な役割を果たしていることを見出した点において学術的重要性がある。さらに、高脂肪食の状況下において造血幹細胞の白血病化の防御に働く因子としてSpred1を特定したことは、幹細胞機能の制御機構を理解する上で重要な知見である。またSpred1の発現低下は白血病発症や増悪化にも関わることから、食生活と白血病発症との関係を考える上で本研究成果の社会的意義は大きいと考えられる。
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