| Project/Area Number |
15K20248
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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 | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 網膜剥離 / 視細胞死 / Fasリガンド / 神経保護 |
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| Outline of Final Research Achievements |
Separation of photoreceptors from underlying retinal pigment epithelium, as seen retinal detachment (RD), causes photoreceptor cell death, resulting in permanent vision loss. In a majority of cases, photoreceptor cell death occurs even if the retina is successfully reattached surgically. Therefore, it is important to define the mechanism(s) of photoreceptor cell death in the detached retina and establish therapeutic targets that prevent photoreceptor loss and the subsequent decrease in visual acuity.
We investigated the role of Fas ligand (FasL) in RD induced photoreceptor cell death using genetically modified mice. Our results showed that FasL induced cell death of photoreceptors following RD. In addition, photoreceptor loss in detached retina was inhibited by a subretinal injection of recombinant soluble FasL. These indicate that treatment targeting FasL could significantly reduce photoreceptor cell loss in patients with RD.
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