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Molecular biological analysis of the Wnt signal pathway in keloid development

Research Project

Project/Area Number 15591906
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Plastic surgery
Research InstitutionNippon Medical School

Principal Investigator

TOSA Mamiko  Nippon Medical School, Medicine, Research Associate, 医学部, 助手 (30301568)

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)
Project Period (FY) 2003 – 2005
Project Status Completed (Fiscal Year 2005)
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)
Keywordskeloid / fibloblasts / Wnt signal / β-catenin / axin / β-catenin / 遺伝子解析 / 線維芽細胞
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.

Report

(4 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • 2003 Annual Research Report
  • Research Products

    (4 results)

All 2005

All Journal Article (4 results)

  • [Journal Article] Global Gene Expression Analysis of Keloid Fibroblasts in Response to Electron Beam Irradiation Reveals the Involvement of Interleukin-6 Pathway2005

    • Author(s)
      Mamiko Tosa
    • Journal Title

      J Invest Dermatol 124

      Pages: 704-713

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Global gene expression analysis of keloid fibroblasts in response to electron beam irradiation reveals the involvement of interleukin-6 pathway2005

    • Author(s)
      Mamiko Tosa
    • Journal Title

      Journal of Investigative Dermatology 124

      Pages: 704-713

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Global Gene Expression Analysis of Keloid Fibroblasts in Response to Electron Beam Irradiation Reveals the Involvement of Interleukin-6 Pathway2005

    • Author(s)
      Mamiko Tosa
    • Journal Title

      Journal of Investigative Dermatology 124

      Pages: 704-713

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Global Gene Expression Analysis of Keloid Fibroblasts in Response to Electron Beam irradiation Reveals the Involvement of Interleukin-6 Pathway2005

    • Author(s)
      Tosa M
    • Journal Title

      Journal of Investigative Dermatology 124

      Pages: 704-713

    • Related Report
      2004 Annual Research Report

URL: 

Published: 2003-04-01   Modified: 2016-04-21  

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