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Clarification of the mechanism of cutaneous inflammation by analyzing the change of redox balance

Research Project

Project/Area Number 15591198
Research Category

Grant-in-Aid for Scientific Research (C)

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

Principal Investigator

YAMAOKA Junichi  Nippon Medical School, Department of Dermatology, Lecturer, 医学部, 講師 (80283688)

Project Period (FY) 2003 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥2,400,000 (Direct Cost: ¥2,400,000)
Keywordsredox balance / oxidative stress / nitric oxide(NO) / apoptosis / cutaneous inflammation / ultraviolet B(UVB) / mouse model / NO / UVB / 虚血再灌流 / モデルマウス / 血管障害
Research Abstract

In the pathogenesis of various cutaneous inflammations, redox balance (balance between oxidative stress and anti-oxidants or anti-oxidative enzymes) is playing essentially important roles. In this research, I tried to clarify the redox balance in the cutaneous inflammation. I focused the research subjects on the following two points.
1,Suppression of ultraviolet B(UVB)-induced keratinocyte apoptosis by moderate doses of nitric oxide(NO).
It is well known that UVB induces keratinocyte apoptosis, in which oxidative stress seems to be involved. I examined the effect of NO on this response. As a result, I found that moderate doses of NO suppress UVB-induced keratinocyte apoptosis. In addition, Moderate doses of NO suppress several molecules in the apoptotic signaling cascades such as p53, caspase 8, caspase 9 and caspase 3, and that NO activates Bcl-2. Through these mechanisms, NO might inhibit UVB-induced keratinocyte apoptosis. However, the reason why NO has this effect is not clear now. It may possibly happen through the reaction of NO to the other redox modulating agents.
2,Development of model mice for the analyses of redox balance in the cutaneous inflammation.
As models which may develop cutaneous inflammation, I made up several model mice for (1)skin ischemia by oppression, (2)skin wound, (3)ultraviolet radiation on the skin, (4)skin scratching. At present, I have just started analyses about redox balance in these model mice. Further analyses will be done to clarify the role of redox balance in the cutaneous inflammation by using these model mice.

Report

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

    (4 results)

All 2004 2003

All Journal Article (4 results)

  • [Journal Article] Nitric oxide inhibits Ultraviolet B-induced murine keratinocyte apoptosis by regulating apoptotic signaling cascades.2004

    • Author(s)
      Junichi Yamaoka, Seiji Kawana, Yoshiki Miyachi
    • Journal Title

      Free Radical Research 38

      Pages: 943-950

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Annual Research Report 2004 Final Research Report Summary
  • [Journal Article] Ultraviolet B-induced murine keratinocyte apoptosis by regulating apoptotic signaling cascades.2004

    • Author(s)
      Junichi Yamaoka, Seiji Kawana, Yoshiki Miyachi
    • Journal Title

      Free Rad Res 36

      Pages: 943-950

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] 紫外線と活性酸素研究:最近のレビュー2003

    • Author(s)
      山岡 淳一
    • Journal Title

      太陽紫外線防御研究委員会学術報告 13

      Pages: 1-9

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Review of the recent research in ultraviolet radiation reactive oxygen species. (Japanese)2003

    • Author(s)
      Junichi Yamaoka
    • Journal Title

      Proceedings of the Japanese Committee for Sunlight Protection 13

      Pages: 1-9

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary

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

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