| Project/Area Number |
16K20242
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Osaka University |
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Principal Investigator |
Imai Ryusuke 大阪大学, 医学部附属病院, 医員 (00747066)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 中耳真珠腫 / 破骨細胞 / RANKL / RNA sequencing / 真珠腫 / RNAシークエンス / 骨破壊 / 伸展圧 / 進展圧 / ケラチノサイト / ファイブロブラスト |
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| Outline of Final Research Achievements |
we found that a significantly larger number of osteoclasts were observed on the eroded bone adjacent to cholesteatomas than in unaffected areas, and that fibroblasts in the cholesteatoma perimatrix expressed RANKL. We also investigated upstream transcription factors of RANKL using RNA sequencing results obtained. The concentrations of four candidate factors were increased in cholesteatomas compared with normal skin. Furthermore, one of these was expressed in infiltrating inflammatory cells in the cholesteatoma perimatrix. This is the first report demonstrating that a larger-than-normal number of osteoclasts are present in cholesteatoma, and that the disease involves upregulation of factors related to osteoclast activation. Our study elucidates the molecular basis underlying bone erosion in cholesteatoma.
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| Academic Significance and Societal Importance of the Research Achievements |
学術的意義として本研究は中耳真珠腫における骨破壊に破骨細胞が関与しているエビデンスの一つとなる。そしてその分子生物学的メカニズムを真珠腫組織のRNA-sequenceによって仮説をあげた。我々の真珠腫モデルマウスを用いた骨破壊抑制実験の足がかりとなると考えられる。臨床的に中耳真珠腫の治療は外科的摘出が唯一の治療法であったが、本研究が示した成果は現在使われている分子学的製剤の点耳薬への応用の可能性を示し、中耳真珠腫の新しい非外科的治療法の開発の根拠となり得る。
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