| Project/Area Number |
24590130
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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 |
Biological pharmacy
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| Research Institution | Setsunan University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KURAMOTO Nobuyuki 摂南大学, 薬学部, 准教授 (60324092)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 神経新生 / 神経変性 / 活性酸素種 / 一酸化窒素 / 海馬歯状回 / 活性酸素 / 神経系幹・前駆細胞 / ニューロン新生 / 活性酸素シグナル / NADPHオキシダーゼ / ニューロン障害 |
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| Outline of Final Research Achievements |
In this study, we evaluated the involvement of nitric oxide (NO)/cGMP pathway in proliferation of NPCs after dentate granule cell loss. NPCs were prepared from the mouse dentate gyrus, nestin-positive cells were cultured for 6 DIV under the same conditions in the absence or presence of NO synthase (NOS) inhibitor Nω-nitro-L-arginine methyl ester (L-NAME), 8-Bromoguanosine 3’, 5’-cyclic monophosphate (8-Br-cGMP), protein kinase G inhibitor KT5823 or NO generator NOC for assessment of cell proliferation. Exposure of the cells to L-NAME significantly attenuated the cell proliferation without morphological change and cell damage. However, the cell proliferation was not affected by 8-Br-cGMP, KT5823, and inactive NOC. By contrast, an exposure to NOC led to a significant increase in the proliferative activity. Taken together, our results support the possibility that NO enhances proliferative activity of the NPCs generated following neuronal loss in the DG independent of cGMP pathway.
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