| Project/Area Number |
18K09377
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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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| Review Section |
Basic Section 56050:Otorhinolaryngology-related
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
北尻 真一郎 信州大学, 学術研究院医学系(医学部附属病院), 特任准教授 (00532970)
山本 典生 京都大学, 医学研究科, 准教授 (70378644)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 内耳 / 有毛細胞 / 難聴 / 細胞内微細構造 / 変性 / 形態異常 / 細胞間接着 / タイトジャンクション / 内耳有毛細胞 / 恒常性 / 細胞変性 |
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| Outline of Final Research Achievements |
To elucidate the mechanism of degeneration of inner ear hair cells, one of the major causes of hearing loss, we focused on inner ear homeostasis. We analyzed genetically engineered mice for structural proteins involved in the cytoskeleton and cell adhesion, which are necessary for maintaining the compartments in the inner ear. One of these proteins, TRIOBP, is involved in the cytoskeletal system. Its deletion causes abnormalities in the shape of the "rootlet" of stereocilia in the hair cells, resulting in deafness. The analysis of these transgenic mice revealed that the rootlet, which had been thought to have a uniform structure, has different domains, providing further insight into the relationship between intracellular microstructure and auditory function.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究において、難聴の表現型を示す、内部環境の維持に必要な細胞骨格や細胞接着関連分子の変異マウスを解析し、細胞内微細構造と聴覚機能の関係について更なる知見を得ることができた。
生体では内耳は骨の中に囲まれている上に、内部環境が厳密にコントロールされているため、その内部環境を壊さず、何か起きているかを調べる事は難しいが、本研究の結果は、ヒト難聴のメカニズムの一端を明らかにしており、難聴治療につながる内耳研究の知識基盤の形成に貢献するものである。
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