| Project/Area Number |
26462563
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Sakaguchi Hirofumi 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (00515223)
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| Co-Investigator(Kenkyū-buntansha) |
宮下 武憲 香川大学, 医学部, 准教授 (60363214)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 内耳 / 蝸牛 / 聴覚 / 有毛細胞 / タイト結合 / 内リンパ / トリセルリン / イオン / tricellulin / 感音難聴 / 遺伝性難聴 / 内リンパ電位 / 難聴 |
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| Outline of Final Research Achievements |
Tricellulin is a member of cell adhesion molecule forming tight junctions and contribute to maintain barrier function in the epithelial cells. We investigated the function of tricellulin in maintaining the ion homeostasis of endolymph, which is extracellular fluid with unique ion component and contained in our sound-sensory organ, inner ears. Genetically engineered tricellulin-deficient mice (Tric-KO mice) show severe hearing loss associated with progressive loss of sensory hair cells during postnatal development. These results revealed the mechanism underlying the onset of sensorineural hearing loss in previously known human hereditary deafness caused by mutations in the tricellulin gene. Moreover, our findings will contribute to elucidate mechanisms of other sensorineural hearing loss caused by compromised ion component and hopefully lead to the development of novel therapeutic approach against deafness by improving the ion homeostasis in the inner ears.
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