| Project/Area Number |
17K11557
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Plastic surgery
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| Research Institution | Nippon Medical School |
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Principal Investigator |
Tosa Mamiko 日本医科大学, 医学部, 准教授 (30301568)
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| Co-Investigator(Kenkyū-buntansha) |
阿部 芳憲 日本医科大学, 先端医学研究所, 助教 (00386153)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | ケロイド / 幹細胞 / ケロイド体質 / 組織幹細胞 / 線維芽細胞 / 治療薬 / 遺伝子発現 / 遺伝子解析 |
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| Outline of Final Research Achievements |
Fibroblasts and stem cells were cultured from (1) redness and (2) ridges (3) normal dermis of keloid patients, and (4) dermis-derived fibroblasts and stem cells of healthy individuals without keloid were used as controls. The A gene was highly expressed in (1), (2), and (3), and when the inhibitor X of the A gene was allowed to act on the cells, a concentration-dependent inhibitory effect was confirmed only in keloid-derived stem cells. These results suggest that gene A is involved in keloid development and that its inhibitor X may be a new therapeutic agent for keloids. In the future, we will analyze other genes related to gene A and aim to establish a more effective external drug for keloid treatment with few side effects.
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| Academic Significance and Societal Importance of the Research Achievements |
Gli1 はヘッジホッグシグナルの標的転写因子である。Gli1 発現は、正常人皮膚では低いのに対して、ケロイド部においては、高発現を認め、興味深いことには、ケロイド患者の正常真皮由来の幹細胞においても高発現を認めたことから、ケロイド発生とケロイド体質決定にGli1 とそれを制御するヘッジホッグシグナルが関与している可能性が非常に高い。研究成果はケロイドの原因解明および新治療の確立につながり、それだけではなく、ケロイド体質診断法の開発創傷治癒メカニズムの解明や癌治療への応用へと発展していく可能性が高く有意義な研究であると考える。
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