| Project/Area Number |
17500255
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Kumamoto University |
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Principal Investigator |
KAGAWA Tetsushi Institute of Molecular Embryology and Genetics, Division of Cell Fate Modulation, Associate Professor, 発生医学研究センター, 助教授 (50270484)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Takashi Institute of Molecular Embryology and Genetics, Division of Cell Fate Modulation, COE research Associate, 発生医学研究センター, COEリサーチアソシエイト (60398237)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | neural stem cells / cell proliferation / undifferentiated state / Wnt / FGF2 / Notch1 / GSK3beta / Hes1 |
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| Research Abstract |
The effects of Wnt signaling on neural progenitor cells were controversial: it was reported to either promote their cell proliferation or accelerate differentiation to become postmitotic neurons. To understand this discrepant role of the Wnt canonical pathway, we applied Wnt3a on the primary culture prepared from embryonic day 15 mouse hippocampus. Wnt3a increased the numbers of total cells, proliferating cells and differentiated neurons. This result phenomenologically suggests that Wnt3a induces both neural progenitor cell proliferation and neuronal differentiation. Notably, the ratio of the number of neurons to total cells after the culture was almost comparable. Wnt3a did not significantly affect the ratio of symmetric and asymmetric cell divisions, but accelerated cell cycle progression by shortening the cell cycle duration, which could result in increases of both proliferative cells and differentiated neurons.
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