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Development of CYP2J2 gene therapy for glomeruonephritis and diabetic nephropathy

Research Project

Project/Area Number 17590832
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Kidney internal medicine
Research InstitutionSaga University

Principal Investigator

MIYAZONO Motoaki  Saga University, Faculty of Medicine, Instructor, 医学部, 助手 (70380780)

Co-Investigator(Kenkyū-buntansha) HIRASE Tetsuaki  Saga University, Faculty of Medicine, Instructor, 医学部, 助手 (60363446)
IKEDA Yuji  Saga University, Faculty of Medicine, Lecturer, 医学部, 講師 (30244023)
ANDO Takashi  Saga University, Faculty of Medicine, Assistant Professor, 医学部, 助教授 (40281191)
NODE Koichi  Saga University, Faculty of Medicine, Professor, 医学部, 教授 (80359950)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Keywordskidney disease / diabetes mellitus / CYP2J2
Research Abstract

CYP2J2 is a crucial regulator of epoxyeicosatrienoic acid production from arachidonic acid. Epoxyeicosatrienoic acid is a vasodilator that relaxes vascular smooth muscle cells and has anti-inflammatory properties against vascular cells. Therefore, it is indicated that induction of CYP2J2 gene in mesangial cells and endothelial cells shows protective effects against kidney by the improvement of blood flow and anti-inflammatory effects.
We studied the effects of angiotensin II, that promotes oxidative stress and inflammation in vascular cells, on CYP2J2 gene expression. We demonstrated increased CYP2J2 mRNA expression in cultured endothelial cells and mesangial cells by RT-PCR. Tumor necrosis factor-a that is an inflammatory cytokine showed similar effects on CYP2J2 mRNA expression in cultured endothelial cells and mesangial cells. These data suggest that inflammatory stimuli increase CYP2J2 mRNA expression in endothelial cells and mesangial cells.
Also, we demonstrated that tumor necrosis factor-α-induced intercellular adhesion molecule-1 expression is decreased by overexpression of CYP2J2 in cultured endothelial cells. This result indicates that CYP2J2 overexpression in endoithelial cells has anti-inflammatory effects.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (5 results)

All 2007 2005

All Journal Article (5 results)

  • [Journal Article] Partial blood recirculation : A new trial for prolonging filter life during continuous hemodiafiltration.2007

    • Author(s)
      Ikeda Y, Kishi T, Kishi C, Miyazono M, Ohtsubo S, Nakashima M, Sakemi T, Ando T, Node K
    • Journal Title

      Ther Aphe (In press)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Partial blood recirculation : A new trial for prolonging filter life during continuous hemodiafiltration.2007

    • Author(s)
      Ikeda Y, Kishi T, Kishi C, Miyazono M, Ohtsubo S, Nakashima M, Sakemi T, Ando T, Node K
    • Journal Title

      Ther Aphe (in press)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] 血管障害への影響2005

    • Author(s)
      野出孝一
    • Journal Title

      糖尿病学の進歩 39集

      Pages: 165-167

    • NAID

      130006952969

    • Related Report
      2005 Annual Research Report
  • [Journal Article] 外因性NO供与の臨床的意義・血管弛緩因子のNOとEETの関係2005

    • Author(s)
      野出孝一
    • Journal Title

      Therapeutic Research 26巻2号

      Pages: 203-212

    • Related Report
      2005 Annual Research Report
  • [Journal Article] 糖尿病患者における心血管合併症の予防と治療 食後高血糖による血管内皮機能の障害とその制御2005

    • Author(s)
      野出孝一
    • Journal Title

      糖尿病合併症 19巻1号

      Pages: 19-21

    • Related Report
      2005 Annual Research Report

URL: 

Published: 2005-04-01   Modified: 2016-04-21  

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