| Project/Area Number |
23592647
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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 | Osaka University |
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Principal Investigator |
INUI Shigeki 大阪大学, 医学(系)研究科(研究院), 寄附講座准教授 (30324750)
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| Co-Investigator(Kenkyū-buntansha) |
ITAMI Satoshi 大阪大学, 大学院医学系研究科, 寄附講座教授 (30136791)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 創傷治癒学 / メラノサイト / Hic-5 / 核内因子 / 増殖 / 運動 / 浸潤 / 細胞増殖因子 / 線維芽細胞 / ケラチノサイト / 創傷治癒 / 表皮 / 皮膚再生 / 分化 |
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| Research Abstract |
The immunocytochemistry revealed that Hic-5 shifts from peri-nuclei to cell membrane during keratinocyte differentiation. Using a stable knockdown HaCat keratinocytes (Hic-5KD-HaCat) and control HaCat (cHaCat), in vitro assays revealed that Hic-5 knockdown suppresses DNA synthesis and accelerates migration more than cHaCat. During HaCat keratinocyte differentiation, keratin 1 expression is suppressed in Hic-5KD-HaCat. Regarding adhesion ability to type IV collagen-coated plates, it was suppressed by Hic-5 knockdown. From these results, Hic-5 plays multipotential functions in growth, differentiation, migration and adhesion of human keratinocytes in wound healing. The 16-F1 murine melanoma cells as a model cell line for normal melanocytes were studied likewise, reveling the potential roles of Hic-5 in the proliferation and motility, suggesting its roles in re-pigmentation during wound healing.
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