| Project/Area Number |
15K10753
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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 | Yamaguchi University |
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Principal Investigator |
SUGAHARA Kazuma 山口大学, 大学院医学系研究科, 准教授 (20346555)
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| Co-Investigator(Kenkyū-buntansha) |
山下 裕司 山口大学, 大学院医学系研究科, 教授 (00210419)
原 浩貴 川崎医科大学, 医学部, 教授 (90274167)
廣瀬 敬信 山口大学, 医学部附属病院, 講師 (80555714)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 内耳 / 内耳有毛細胞 / 内耳感覚細胞障害 / 卵形嚢培養 |
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| Outline of Final Research Achievements |
When inner ear sensory cells are damaged, activation of molecules involved in intracellular signal transduction is induced, and then sensory cells are killed. Mammalian sensory cells are not regenerated once they are impaired, and they constitute a barrier to the current treatment of deafness. In this study, we focused on mitochondria in inner ear sensory cells. We tried to introduce molecular biological techniques using RNA as a means.
As a result, we also clarified that protecting mitochondrial function in inner ear sensory cells can suppress cell damage. Although it was difficult to construct in vivo animal models, models using other drugs were constructed and reported in English.
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| Academic Significance and Societal Importance of the Research Achievements |
内耳感覚細胞死のメカニズムは最近の研究で明らかになりつつあるが，まだ治療方法として確立されたものはない。本研究は動物実験のレベルであるが，これまでに報告されていない手段を用いて，内耳感覚細胞を保護できることを示した。さらに研究が進展することで，内耳疾患の新しい治療法の一手段につながることを期待している。
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