Regulation of Nell2 in the senescence-accelerated mouse andelucidation of axonal extension.
| Project/Area Number |
23792016
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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 |
Ophthalmology
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 網膜 / 老化 / 神経 / 緑内障 / 網膜神経節細胞 / 視神経 |
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| Research Abstract |
The senescence-accelerated mouse (SAM) has been established as a model of accelerated aging. SAM consists of the senescence-accelerated prone mouse (SAMP) and senescence-accelerated resistant mouse (SAMR), which exhibits normal aging process. We investigated the change of retinal ganglion cell (RGC) and Sirtuin 1 (Sirt1), which is a member of the sirtuin family of proteins and related with aging process, and Nell2, which is involved in neuronal growth process, in SAMR, SAMP8, and SAMP10. RGC in3 month old SAMP8 and P10 was significantly decreased, compared with those in SAMR. No significant changes in the INL and the ONL were observed in SAMR, SAMP8, and SAMP10. IB showed that a significant decrease in Sirt1 and Nell2 were observed in the retinas of SAMP8 and SAMP10, compared to SAMR. An abundant Sirt1 was seen in the RGC and the IPLof SAMR retina, compared to those in SAMP8 and SAMP10.
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Report
(3 results)
Research Products
(17 results)
