| Project/Area Number |
15591906
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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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 Nippon Medical School, Medicine, Research Associate, 医学部, 助手 (30301568)
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| Co-Investigator(Kenkyū-buntansha) |
GHAZIZADEH Mohammad Nippon Medical School, Institute of Gerontlogy, Associate Professor, 老人病研究所, 助教授 (30190979)
KAWANAMI Oichi Nippon Medical School, Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (70096973)
MURAKAMI Masahiro Nippon medical School, Medicine, Associate Professor, 医学部, 助教授 (00239500)
平井 隆 日本医科大学, 医学部, 助教授 (40208799)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | keloid / fibloblasts / Wnt signal / β-catenin / axin / β-catenin / 遺伝子解析 / 線維芽細胞 |
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| Research Abstract |
Keloid is a dermal fibroproliferative lesion of unknown etiology. Wnt signaling pathway plays an important role in the regulation of cell growth and differentiation. Activation of Wnt signaling pathway in keloid fibroblasts (KF) is thought to be closely linked to abnormal cell proliferation and migration. We first examined the difference in mRNA expression of downstream targets in the Wnt signaling pathway namely β-catenin and axin between keloid fibroblasts and normal dermal fibroblasts (NF). The β-catenin was overexpressed in KF, although axin, an inhibitory gene to β-catenin, was suppressed in KF. Immunohistochemical analysis confirmed the high expression of β-catenin and low expression of axin in KF. To examine the functional properties of the Wnt signaling pathway, we then investigated extracellular matrix (ECM) related gene expression in both NF and KF.
We measured mRNA expressions of two principal ECM molecules, COL1A2 and FN1, in KF and NF after treatment with a β-catenin peptide. COL1A2 and FN1 mRNA expressions after addition of β-catenin peptide were increased in both NF and KF. These findings suggested the involvement of activated Wnt signal pathway in the pathogenesis of keloid sacr via enhancing the ECM-related gene expression in fibroblasts.
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