| Project/Area Number |
17K16968
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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 |
Ophthalmology
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| Research Institution | Osaka University |
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Principal Investigator |
Hara Susumu 大阪大学, 医学系研究科, 助教 (00536956)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | 角膜内皮 / TFAP2B / 転写因子 / STAT3 / バリア機能 / ZO-1 / 角膜 / 転写制御 / TFAP2ファミリー / 発現制御 |
|---|
| Outline of Final Research Achievements |
We have previously demonstrated the role played by TFAP2B in the development and proliferation of corneal endothelial cells. In this study, using drug screening, we identified STAT3 as a transcription factor that can regulate the expression of TFAP2B. We found that STAT3 signaling regulates corneal endothelial cell survival and barrier function, a major function of these cells, suggesting that TFAP2B in cooperation with STAT3 regulates corneal endothelial cell homeostasis.
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| Academic Significance and Societal Importance of the Research Achievements |
角膜内皮はポンプ機能およびバリア機能によって角膜の透明性を維持する上で重要な組織である。本研究において、角膜内皮のバリア機能とTFAP2BおよびSTAT3の関連について示した。角膜内皮の主要なバリア機能における転写制御機構の解明によって、角膜内皮疾患の発症メカニズムの解明や角膜内皮の再生医療分野において有用であると考えられる。
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