| Project/Area Number |
26861032
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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 |
Radiation science
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| Research Institution | National Institute of Radiological Sciences |
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Principal Investigator |
Tomiyama Ken-ichi 国立研究開発法人放射線医学総合研究所, 緊急被ばく医療研究センター, 博士研究員 (20584064)
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| Co-Investigator(Renkei-kenkyūsha) |
Obara Chizuka 国立研究開発法人放射線医学総合研究所, 緊急被ばく医療研究センター, 研究員 (90415977)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | radiation injure / BDNF / IEC-6 / MSC / radiation / apoptosis / 放射線障害 / 細胞死 |
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| Outline of Final Research Achievements |
Here, we demonstrate that brain-derived neurotrophic factor (BDNF), an endogenous ligand for tyrosine kinase B (TrkB) receptor, protect IEC-6 cells against gamma (γ)-irradiation damage. IEC-6 was exposed with 4Gy of γ-irradiation and then challenged BDNF treatment. After 24 hours, γ-irradiation-induced cell death of IEC-6 and expression of cleaved caspase-3 were decreased. Further examination shows that BDNF suppresses apoptosis of IEC-6 induced by irradiation damage through an increase of Bcl-2/Bax ratio. BDNF significantly enhanced the phosphorylation of Akt and ERK1/2 proteins by subsequent to irradiation and ameliorated the expression of Bcl-2 protein. These data also indicates that PI3K/AKT and/or ERK1/2 pathway activated by BDNF plays important role for IEC-6 survival after γ-irradiation. Therefore, BDNF may be therapeutically useful to attenuate the intestinal injury caused by radiation.
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