| Project/Area Number |
14370552
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Hirosaki University |
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Principal Investigator |
NAKAZAWA Mitsuru Hirosaki University, School of Medicine, Professor, 医学部, 教授 (80180272)
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| Co-Investigator(Kenkyū-buntansha) |
OHGURO Hiroshi Hirosaki University, School of Medicine, Associate Professor, 医学部, 助教授 (30203748)
ISHIGURO Seiichi Hirosaki University, School of Agriculture and Biological Science, Professor, 農学生命科学部, 教授 (20111271)
OHGURO Ikuyo Hirosaki University, School of Medicine, Assistant Professor, 医学部, 講師 (90305235)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥14,700,000 (Direct Cost: ¥14,700,000)
Fiscal Year 2004: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥7,700,000 (Direct Cost: ¥7,700,000)
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| Keywords | retinitis pigmentosa / GCAP2 gene / calcium antagonist / GCAP2遺伝子 / アントシアニン / カルシウム拮抗剤 |
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| Research Abstract |
The aims of this research project are to investigate responsible genes for hereditary retinal degeneration namely retinitis pigmentosa and to examine the possibility for novel medical treatments for these diseases based on the findings of molecular pathogenesis that would be obtained by the molecular genetic analyzes.
As for the first point, i. e. molecular genetic analysis for retinitis pigmentosa and allied diseases, we have first reported that the GCAP2 gene is one of the responsible genes for retinitis pigmentosa based on the findings that we had identified the same mutation in the GCAP2 gene in the affected members of three independent Japanese families (Sato, Nakazawa, et al.,2005). We had focused on this gene as a candidate gene for retinitis pigmentosa for more than 5 years. Moreover, the further genotype-and-phenotype study revealed that this particular mutation was associated with not only typical retinitis pigmentosa, but also retinitis pigmentosa associated with macular dege
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neration or solely macular degeneration, suggesting that the mutation in the GCAP2 gene may be related to genetic heterogeneity. In addition, because GCAP2 protein is a kind of calcium-binding protein, it is also suggested that calcium ion may play a certain role when retinal degeneration occurs in relation to the mutation in the GCAP2 gene.
As for the second point, i. e. novel medical treatment for retinitis pigmentosa, we have already reported the experimental therapeutic effects of calcium antagonist on retinal degeneration of RCS rats and rd (retinal degeneration) mouse (Takano, Nakazawa, et al.,2004). These experimental animal studies favorably suggest the possibility that some of calcium antagonists may play as a photoreceptor-protective agents for retinitis pigmentosa. We further examined the effect of antocyanine on experimental retinal degeneration. Results indicate that it delays retinal degeneration of RCS rats electrophsyolosically. These results suggest further availability of antocyanine as a thrapeutic agent for retinitis pigmentosa. Less
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