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Mitochondria injuries of Peritoneal Mesothelial Cells induced by oxidative stress

Research Project

Project/Area Number 13671131
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Kidney internal medicine
Research InstitutionKAWASAKI MEDICAL SCHOOL

Principal Investigator

SASAKI Tamaki  Kawasaki Medical School Medicine Associate Professor, 医学部, 助教授 (30187124)

Co-Investigator(Kenkyū-buntansha) SHINDO Akihisa  Kawasaki Medical School Medicine Assistant Professor, 医学部, 講師 (00278920)
KASHIHARA Naoki  Kawasaki Medical School Medicine Professor, 医学部, 教授 (10233701)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
KeywordsPeritoneum / Mesothelial cell / Oxidative stress / Mitochondria / Angiogenesis / Klotho mouse / 8-OHdG / 硬化性腹膜炎
Research Abstract

Oxidative stress by reactive oxygen species (ROS) is thought to be involved in the pathogenesis of various diseases. The pathological effect of oxidative stress on the peritoneum was studied basically with 8- OHdG. Immunohistochemical staining of 8- OHdG was weakly detected in the mesothelial cells of the healthy control, whereas strong staining was observed in the mesothelial cells and vascular walls of patients with sclerosing peritonitis. The presence of 8- OHdG in infiltrative cells in peritonitis was confirmed. The 8- OHdG levels in CAPD solution increased in proportion to the duration of dialysis irrespective of age, and they were high in the patients with peritonitis. Thereforem the 8- OHdG level in CAPD solutions might possibly be used as a clinical marker of inflammttion of the peritoneum and impairment of mesothelial cells
Subsequently, the effect of a high glucose concentration (HG group, 214mM) on rat culture mesothelial cells was investigated. The ROS production was visuali … More zed and checked by Dichlorofluorescein diacetat. Upon exposure to HG, the mesothelial cells produced more ROS than those of the control group. These results suggest that the mitochondria were extremely vulnerable to oxidative stress because they were a major intracellular source of ROS
Next, neoangiogenesis during acute peritonitis was investigated morphologically. Fluorescent Griffonia simplicifolia 1 lectin was used to visualize the pattern of capillaries in the peritoneum by laser scanning confocal microscopy. Branching anastomoses between the parallel parent capillaries formed an irregular lace- like meshwork rather than individual straight interconnections. In the peritonitis model rats, cell infiltration was recognized on the surface of the peritoneum, and some of these cells expressed CD34. Immunohistocemistry revealed expression of Flk-1, Flt-1, and Tie-2 in these cells. These results may represent a new and promising strategy for dealing with peritoneal dysfunction by clinical application to new vessel formation Less

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (17 results)

All Other

All Publications (17 results)

  • [Publications] Tamaki Sasaki, et al.: "Infiltrating mononuclear cells augment new vessel formation during acute peritonitis"J Am Soc Nephrol. 12. 456A (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tamaki Sasaki, et al.: "Mitochondria of mesothelial cells is major intracellular source of ROS during CAPD"J Am Soc Nephrol. 12. 310A (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tatsuo Fukushima, et al.: "Accumulation of oxidative DNA damage and hOGG1 polymorphism are correlated with pathogenesis of diabetic nephropathy"J Am Soc Nephrol. 12. 146A (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hideyuki Horike, et al.: "The Role of Mitochondria in the Angiogenesis for Repairing the Interstitial Iniuries"J Am Soc Nephrol. 13. 164A (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hideyuki Horike, et al.: "Impaired Angiogenesis in the Development of Interstitial Fibrosis in the Progressive Renal Diseases"J Am Soc Nephrol. 13. 164A (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tamaki Sasaki, et al: "Infiltrating Mononuclear Cells Augment New Vessel Formation During Acute Peritonitis"J Am Soc Nephrol. 12: 456A. (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tamaki Sasaki, et al: "Mitochondria of Mesothelial Cells is Major Intracellular Source of ROS During CAPD"J Am Soc Nephrol. 12: 310A. (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tatsuo Fukushima, et al: "Accumulation of Oxidative DNA Damage and hOGGl Polymorphism are Correlated with Pathogenesis of Diabetic Nephropathy"J Am Soc Nephrol. 12: 146A. (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hideyuki Horike, et al: "The role of Mitochondria in the Angiogenesis for Repairing the Interstitial Injuries"J Am Soc Nephrol. 13: 164A. (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hideyuki Horike, et al: "Impaired Angiogenesis in the Development of Intersitital Fibrosis in the Progressive Renal Disease"J Am Soc Nephrol. 13: 164A. (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Sohachi Fujimoto, et al.: "The Role of Angiotensin II in the Generation of Oxidative Stress in Progressive Renal Diseases : Effects of ACEI and ARB"J Am Soc Nephrol. 13. 155A (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Hideyuki Horike, et al.: "Impaired Angiogenesis in the Development of Intersitial Fibrosis in the Progressive Renal Diseases"J Am Soc Nephrol. 13. 164A (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Hideyuki Horike, et al.: "The Role of Mitochondria in the Angiogenesis for Repairing the Interstitial Injuries"J Am Soc Nephrol. 13. 164A (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Minoru Satoh, et al.: "Novel Free Radical Scavenger, MCI-186, Protects Cisplatin-Induced Acute Renal Damage In Vitro and In Vivo"J Am Soc Nephrol. 13. 546A (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] T SASAKI, et al.: "Infiltrating mononuclear cells augment new vessel formation during acute peritonitis"J Am Soc Nephrol. 12. 456AI (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] T SASAKI, et al.: "Mitochondria of mesothelial cells is major intracellular source of ROS during CAPD"J Am Soc Nephrol. 12. 310A (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] T FUKUSHIMA, et al.: "Accumulation of oxidative DNA damage and hOGGl polymorphism are correlated with pathogenesis of diabetic nephropathy"J Am Soc Nephrol. 12. 146A (2001)

    • Related Report
      2001 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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