| Project/Area Number |
18K16906
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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 | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ミトコンドリア / 動的評価 / 細胞骨格 / PQQ / 老化 / 拡散係数 / 蝸牛 / 有毛細胞 |
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| Outline of Final Research Achievements |
The mitochondrial movement in the cochlea cell line (HEI-OC1) was continuously tracked by extracting feature points and calculating optical flow using OpenCV, calculating diffusion coefficients, etc. The same coefficients were calculated after exposure to cytoskeletal inhibitors, and dynamic evaluation was performed. The mitochondrial membrane potential was evaluated by plate reader and fluorescence microscopy. The morphology of mitochondria was evaluated by electron microscopy. After exposure to PQQ (0.1, 1.0 nM) for 1 day, the cells were exposed to hydrogen peroxide (100 μM) for 1 hour to evaluate mitochondrial function and mitochondrial area. SIRT1/PGC-1α pathway functions were evaluated.
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| Academic Significance and Societal Importance of the Research Achievements |
蝸牛培養細胞株（HEI-OC1）老化モデルでのミトコンドリア呼吸能、ATP産生速度、ミトコンドリア膜電位・融合・運動性の障害はPQQ処理群で保護され、SIRT1及びPGC-1αの発現は有意に上昇し、PGC-1αのアセチル化は有意に減少した。ミトコンドリア拡散係数が増加する傾向にあり、動的な側面が改善する可能性が示唆された。
細胞老化においてPQQにより細胞骨格の観点からの評価を含めたミトコンドリア機能が改善することが示唆され、加齢性難聴に対して有効な薬剤であることが推測され、同内容にて特許出願を行った。本内容は、高齢化社会における難聴予防の点からも学術的意義や社会的意義があると考えられる。
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