| Project/Area Number |
20K18419
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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 56070:Plastic and reconstructive surgery-related
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| Research Institution | Keio University |
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Principal Investigator |
IKURA Naohiko 慶應義塾大学, 医学部(信濃町), 助教 (10867758)
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| Project Period (FY) |
2020-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2021: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2020: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | YAP / TAZ / ケロイド / 肥厚性瘢痕 / YAP/TAZ |
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| Outline of Research at the Start |
YAP/TAZの検討を行い、ケロイドの病態形成にYAP/TAZが関与する機械的シグナルが関与している可能性を検討し、そのシグナルを阻害することで将来的な治療への応用を目指す。
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| Outline of Final Research Achievements |
In human keloid tissue, the nuclear translocation rate of YAP / TAZ was significantly increased in lesion fibroblasts compared to normal skin at the margin, whereas the nuclear translocation rate was no significant difference in vascular endothelial cells and in epidermal cells. These data suggested that fibroblasts may be involved in the keloid tissue hardness signal. Furthermore, in the mouse back scar model, the nuclear translocation rate of YAP / TAZ in fibroblasts was higher than that of the control group, similar to the result of human tissue. In the future, we plan to investigate the possibility of application to treatment with YAP / TAZ nuclear translocation inhibitors.
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| Academic Significance and Societal Importance of the Research Achievements |
ケロイド組織やマウス瘢痕モデルでも線維芽細胞におけるYAP/TAZの核内移行が認められたことから、持続する炎症や病変拡大に線維芽細胞のYAP/TAZシグナルが関与している可能性が示唆され、また核内移行阻害薬を用いることでケロイド治療に発展する可能性が考えられた。
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