| Project/Area Number |
23650163
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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 |
Neuroscience in general
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| Research Institution | Kanazawa University |
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Principal Investigator |
KATO Satoru 金沢大学, 医学系, 教授 (10019614)
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| Co-Investigator(Renkei-kenkyūsha) |
TANII Hideji 金沢大学, 医学系, 准教授 (90110618)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 魚 / 視神経再生 / sox2 / klf4 / c-myc / oct3/4 / 神経幹細胞 / 神経損傷 / 山中因子 / ネスチン / LIF / ゼブラフィッシュ / 網膜神経節細胞 / ｋｌｆ4 |
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| Research Abstract |
Unlike mammals, fish optic nerve can regenerate after nerve injury. We have a hypothesis of this regenerative capacity of fish optic nerve that mature retinal ganglion cells (RGCs) in fish are reprogrammed to neural stem-cell like cells by optic nerve injury. To certain this hypothesis, we investigated expression levels of sox2, klf4, c-myc and nestin in the zebrafish retina after optic nerve injury. The levels of sox2, klf4 and c-myc mRNA increased in the retina 3 days after axotomy. The level of a neural stem cell marker, nestin increased in the retina 4-5 days after axotomy. These molecules were all localized to the RGCs. Furthermore, we found that leukemia inhibitory factor (LIF) was positional as an upstream signal to the klf4 and sox2. In the presence of LIF in culture medium of retinal explant, a significant neurite outgrowth could be seen as compared to the no treatment, control. In contrast, the inhibition of LIF signals leaded to the suppression of neurite outgrowth from retina. Therefore, we conclude that the capability of fish optic nerve regeneration is due to reprograming mechanism of matured RGCs after optic nerve injury.
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