Is mitochondrial dysfunction related to delayed neuronal cell death after radiation exposure?
| Project/Area Number |
25861113
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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 | Oita University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 電離放射線 / ミトコンドリア形態 / 神経変性 / 遅発性活性酸素種 / Drp1タンパク質 / 神経軸索 / カルシウムシグナル / 遅延的影響 / ガンマ線 / 活性酸素種 / 細胞死 |
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| Outline of Final Research Achievements |
Recently it is reported that mitochondrial dynamics may contribute to function of the neuron. However, little is known about the radiation-induced mitochondrial fragmentation in these neurons, especially in axons.We examined the effects of radiation exposure on rat primary neuron. We found radiation exposure induced elongation of the axon. To study the effect of mitochondrial fission on shape of neuron after irradiation, we knock down central mitochondrial fission protein, Drp1 protein expression. The neuron knock down Drp1 expression did not elongate axon after gamma-irradiation.
As a result, promotion of mitochondrial fission after irradiation may effect on axon elongation after exposure.
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Report
(3 results)
Research Products
(11 results)
