| Project/Area Number |
18K16876
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56050:Otorhinolaryngology-related
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Keiji Honda 東京医科歯科大学, 医学部附属病院, 助教 (90621079)
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 内リンパ嚢 / イオノサイト / 細胞分化 / 前庭水管拡大 / 先天性難聴 / 組織培養 / Notchシグナル伝達系 |
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| Outline of Final Research Achievements |
The endolymphatic sac is essential for the normal development and function of the inner ear, and its abnormality causes inner ear diseases such as enlarged vestibular aqueduct. To elucidate the cell differentiation mechanism of mitochondria-rich cells and ribosome-rich cells, which are the two cell types constituting the endolymphatic sac, we attempted to observe the effects of knockdown of candidate genes for transcriptional regulation on cell differentiation in mouse endolymphatic sac tissue culture. Although we tried various protocols, contraction of epithelial tissues occurred during culture of the endolymphatic sac, leading to problems in maintaining a stable morphology that could be examined under a microscope. It is thought that ion transport and water absorption by MRC may have affected the morphology of the cells.
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| Academic Significance and Societal Importance of the Research Achievements |
内リンパ嚢細胞の分化機構の解明は前庭水管拡大症の治療法の確立に極めて重要な意義を持つ。たとえば、イオン輸送関連遺伝子の変異によりタンパクレベルでイオン輸送機能低下を有している場合においても、前駆細胞からMRCへの分化を誘導させその細胞数を増加させることによって、機能低下を補完できる可能性がある。また別の可能性として、ES/iPS細胞からMRCに分化誘導する手法を構築し、治療へつなげることも考えられる。
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