| Project/Area Number |
18K08271
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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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| Review Section |
Basic Section 53050:Dermatology-related
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| Research Institution | Nagasaki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
岩永 聰 長崎大学, 医歯薬学総合研究科(医学系), 助教 (00621947)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ケロイド / HDAC阻害剤 / エピジェネティクス |
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| Outline of Final Research Achievements |
We examined the gene expressions of extracellular matrix and transcription factors in keloid cells with HDAC inhibitor in vitro. Previously, we found HDAC2 was upregulated in the keloid tisuue, therefore, we choose Mocetinostat, Apicidin and CAY10683 which are selective HDAC2 inhibitor. As a result, any HDAC inhibitors could inhibit the COL1A2 mRNA expressions, especially mocetinostat could inhibit TGF-β1 greater extent. Moreover, higher gene expressions were detected in the MMP-1,3. These suggests mocetinostat control several transcriptional factors and improve keloid fibrosis in the keloid. More number of the studies and further mechanism examination would be needed.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の検討により、HDAC２を選択的に阻害する薬剤は、ケロイドの過剰な膠原線維産生などを抑制する可能性が見いだされた。今回検討した、ApicidinやMocetinostatなどは既に他疾患領域で内服薬として治験が行われており、安全性や使用法などが確立されつつある。さらなる検証を加え、より安全かつ低侵襲な治療法に応用可能な薬剤の開発に寄与してゆきたい。
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