| Project/Area Number |
16K12599
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Risk sciences of radiation and chemicals
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
Kodak Seiji 大阪府立大学, 理学(系)研究科(研究院), 教授 (00195744)
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| Co-Investigator(Renkei-kenkyūsha) |
SHIRAISHI Kazunori 大阪府立大学, 理学系研究科生物科学専攻, 助教 (40347513)
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| Research Collaborator |
KASHIWAGI Hiroki 大阪府立大学, 理学系研究科生物科学専攻, 客員研究員
SAKAGUCHI Kenta 大阪府立大学, 理学系研究科生物科学専攻, 客員研究員
OIE Ayaka 大阪府立大学, 理学系研究科生物科学専攻
KANABOSHI Sakura 大阪府立大学, 理学系研究科生物科学専攻
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ニューロン / 神経幹/前駆細胞 / DNA２本鎖切断 / 非相同末端結合 / DNA依存的プロテインキナーゼ / アポトーシス / DNA２本鎖切断修復 / DNA2本鎖切断 / 神経系発生 / 損傷 / 神経系細胞 |
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| Outline of Final Research Achievements |
We investigated the repair kinetics of X-ray-induced DNA double-strand beaks (DSBs) in mouse neural stem/progenitor cells (NSPCs) and their differentiated neurons by scoring the number of phosphorylated histone H2AX (gamma-H2AX) foci or phosphorylated 53BP1 foci post-irradiation. The DSB repair in neurons differentiated from NSPCs in culture was faster than that in mouse embryonic fibroblasts (MEFs), possibly due to the higher DNA-dependent protein kinase activity, but similar to that in NSPCs. Further, the incidence of p53-dependent apoptosis induced by X-irradiation in neurons was significantly higher than that in NSPCs. This difference in response of X-ray-induced apoptosis between neurons and NSPCs may reflect the difference in the fidelity of non-homologous end joining or the differential sensitivity to DNA damage other than DSBs.
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