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The Research on the ion channels which are involved in the cytoprotective medianisms of endothelial cells in the atherosclerotic model animal

Research Project

Project/Area Number 18590206
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field General physiology
Research InstitutionFukushima Medical University

Principal Investigator

HAZAMA Akihiro  Fukushima Medical University, School of Medicine, Professor (60218394)

Co-Investigator(Kenkyū-buntansha) KATSUDA Shin-ichiro  Fukushima Medical University, School of Medicine, Lecturer (80285022)
YAMASAKI Masao  Fukushima Medical University, School of Medicine, Associate Professor (10192395)
MIYAKE Masao  Fukushima Medical University, school of Medicine, Research Associate (00381385)
Project Period (FY) 2006 – 2007
Project Status Completed (Fiscal Year 2007)
Budget Amount *help
¥3,930,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
Keywordsatherosclerosis / Cl-channel / endothelial cells / amphotericin B / cvto-protection / ion channel / high NaC1 diet / Cl-channel blocker / 細胞障害 / 塩素シオン / 塩素イオン
Research Abstract

We established the primary culture of the endothelial cells from rabbits. We examined the role of ion channels in the cytoprotective effects. We applied amphotericin B on the endothelial cells which caused cell damage by the enhancement of the membrane permeability and tested different ionic conditions and ion channel blockers. We found that Cl- channel blockers, NPPB and DIDS, inhibited endothelial cell damage caused by amphotericin B. We also found that Cl- replacement by other organic anions suppressed cell-damage by amphotericin B. Cellular damage caused by hydrogen peroxide was also inhibited by Cl- channel blockers or Cl- free conditions. These results suggest that Cl- influx via Cl- channels might cause the endothelial cell damage during the formation of atherosclerosis. To access this question, we applied high NaC1 diet to the atherosclerosis model rabbit (KHC rabbit) for 6 months to check the formation of atherosclerosis. Surprisingly we found. that the formation of atherosclerosis was suppressed by the high NaC1 diet. We are investigating the mechanisms of this effect.

Report

(3 results)
  • 2007 Annual Research Report   Final Research Report Summary
  • 2006 Annual Research Report
  • Research Products

    (4 results)

All 2008 2007

All Journal Article (4 results) (of which Peer Reviewed: 1 results)

  • [Journal Article] Deep-sea water improves cardiovascular hemodynamics in Kurosawa and Kusanagi-Hypercholesterolemic (KHC) rabbits2008

    • Author(s)
      Katsuda S, Yasukawa T, Nakagawa K, Miyake M, Yamasaki M, Katahira K, MohriM, Shimizu T, Hazama A.
    • Journal Title

      Biological & pharmaceutical bulletin 31

      Pages: 38-44

    • NAID

      110006569971

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2007 Final Research Report Summary
    • Peer Reviewed
  • [Journal Article] Deep-sea water improves cardiovascular hemodynamics in Kurosawa and Kusanagi-Hypercholesterolemic (KHC) rabbits2008

    • Author(s)
      Katsuda, S., Yasukawa, T., Nakagawa, K., Miyake, M., Yamasaki, M., Katahira, K., Mohri, M., Shimizu, T., Hazama, A
    • Journal Title

      Biol Pharm Bull 31

      Pages: 38-44

    • NAID

      110006569971

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2007 Final Research Report Summary
  • [Journal Article] Deep-sea water improves cardiovascular hemodynamics in Kurosawa and Kusanagi-Hypercholesterolemic (KHC) rabbits.2008

    • Author(s)
      Katsuda S, Yasukawa T, Nakagawa K, Miyake M, Yamasaki M, Katahira K, Mohri M, Shimizu T, Hazama A.
    • Journal Title

      Biological & pharmaceutical bulletin 31

      Pages: 38-44

    • NAID

      110006569971

    • Related Report
      2007 Annual Research Report
  • [Journal Article] Potential of heterotopic fibroblasts as autologous transplanted cells for tracheal epithelial regeneration.2007

    • Author(s)
      Kobayashi K, Suzuki T, Nomoto Y, Tada Y, Miyake M, Hazama A, Nakamura T, Omori K.
    • Journal Title

      Tissue engineering 13

      Pages: 2175-2184

    • Related Report
      2007 Annual Research Report

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Published: 2006-04-01   Modified: 2016-04-21  

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