| Project/Area Number |
15K10760
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
御子柴 克彦 国立研究開発法人理化学研究所, 脳神経科学研究センター, チームリーダー (30051840)
河原 克雅 北里大学, 医学部, 名誉教授 (70134525)
阪上 洋行 北里大学, 医学部, 教授 (90261528)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | IP3受容体type1 / IP3受容体type1KOマウス / Boettcher細胞 / 小胞体ストレス / 蝸牛機能 / 聴覚 / IP3受容体 / 外らせん溝細胞 |
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| Outline of Final Research Achievements |
The present study was the first report to confirm that the Inositol trisphosphate receptor type-1 (IP3 receptor type1) was observed in the cochlea and the hearing was impaired in IP3 receptor type1 KO mice, furthermore, in the homo (-/-) mice, the endoplasmic reticulum in Boettcher cell was severely swollen. This severely swollen endoplasmic reticulum in Boettcher cell may be induced by accumulation of abnormal protein (ER stress) which may be due to a deficiency in the function of IP3 receptor type 1.
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| Academic Significance and Societal Importance of the Research Achievements |
環境ストレスが内耳性難聴を生じさせるメカニズムの一端が解明されたことになる。このことは、メニエール病・突発性難聴などの内耳性難聴が、ストレスと強い関連性があることの解明に貢献したと考えられる。
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