2010 Fiscal Year Final Research Report
Retinal ganglion cell loss in superoxide dismutase 1-deficiency
| Project/Area Number |
21791714
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Keio University |
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Principal Investigator |
OZEKI Naoki Keio University, 医学部, 助教 (80383826)
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| Project Period (FY) |
2009 – 2010
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| Keywords | 酸化ストレス / 緑内障 / superoxide dismutase 1 / 網膜神経節細胞 / 網膜電図 |
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| Research Abstract |
Purpose. To investigate the influence of deficiency in superoxide dismutase 1 (SOD1), a major antioxidative enzyme, on retinal ganglion cells (RGCs). Methods. In the SOD1 total knock-out (SOD1-deficient) mice, the level of superoxide anion was measured using dihydroethidium. The number of RGCs was counted both in the retinal sections and the flat-mount retinas after retrograde labeling. Thickness of nerve fiber layer (NFL) was measured in the sections and the amount of neurofilament protein was measured by immunoblot analysis. Pattern electroretinogram (ERG) which reflects the function of retinal ganglion cells, dark-adapted ERG, and cone ERG were performed. The intraocular pressure (IOP) was measured with an induction-impact tonometer. Results. The level of superoxide anion in the RGC layer was significantly higher in 24-week-old SOD1-deficient mice than in wild-type mice. The RGC number was significantly reduced in 24-week-old SOD1-deficient mice, although they were not in 8-week-old mice. The NFL thickness and neurofilament protein were reduced in 24-week-old SOD1-deficient mice. The amplitude of pattern ERG was significantly reduced, although dark-adapted and cone ERGs showed no impairment, in 24-week-old SOD1-deficient mice. The IOP level was not changed in the SOD1-deficient mice.
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