| Project/Area Number |
17K16190
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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 |
Hematology
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| Research Institution | Kumamoto University |
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Principal Investigator |
Umemoto Terumasa 熊本大学, 国際先端医学研究機構, 特任助教 (50620225)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 造血幹細胞 |
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| Outline of Final Research Achievements |
So far, it is thought that HSCs are maintained by suppressing cell divisions. In this study, we suggested that IFNγis unable to maintain HSCs through the activation of energy metabolism while this cytokine suppresses HSC divisions. In addition, the appropriate suppression of energy metabolism contributes to HSC maintenance after cell divisions. Therefore, it is expected to clarified the mechanism how energy metabolism contributes to HSC divisions and the maintenance of stem-ness.
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| Academic Significance and Societal Importance of the Research Achievements |
これまで、「造血幹細胞は維持するためには分裂をさせない」と考えられてきたが、本研究において、分裂抑制をしても幹細胞を維持出来ないメカニズム、さらには造血幹細胞が分裂後に幹細胞性を維持するメカニズムの一端を見出すことが出来た。これらの成果は、造血幹細胞の体外増幅技術の開発に大きく寄与し、骨髄移植を用いた遺伝子治療や再生医療の発展に大きく寄与すると考えられる。
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