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2001 Fiscal Year Final Research Report Summary

RESEACH FOR THE PATHOGENESIS OF DIABETIC RETINOPATHY

Research Project

Project/Area Number 12671106
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Metabolomics
Research InstitutionNagoya University

Principal Investigator

HAMADA Yoji  University Hospital, Nagoya University, Research Associate, 医学部・附属病院, 助手 (20293706)

Co-Investigator(Kenkyū-buntansha) NAKASHIMA Eitaro  University Hospital, Nagoya University, Research Associate, 医学部・附属病院, 助手 (50335030)
NAKAMURA Jiro  Graduate School of Medicine, Nagoya University, Associate Professor, 大学院・医学研究科, 助教授 (40283444)
Project Period (FY) 2000 – 2001
KeywordsDiabetic Complications / Retinal MicrovascuLar Pericytes / Apoptosis / Poiyol Pahtway / Protein Kinase C / Oxidentive Stress / Aldose Reductase Inhibitior
Research Abstract

The mechanisms of the glucose-induced apoptosis in retinal pericytes were investigated to evaluate the pathogenesis of diabetic retinopathy. Under the 20 mM glucose condition, intracellular calcium concentrations and caspase-3 activities were significantly increased, and reduced glutathione contents and PKC activities were significantly decreased, compared with those under the 5. 5 mM glucose condition. These abnormalities were all significantly prevented by an aldose reductase inhibitor, SNK-860. Glucose-induced apoptosis was partially but significantly prevented by SNK-860, a calpain inhibitor, or reduced glutathione supplementation, and completely normalized by a caspase-3 inhibitor. These observations suggest that glucose-induced apoptosis in retinal pericytes would be mediated through an aldose reductase sensitive pathway including caicium-calpain cascade, increased oxidative stress and decreased PKC activities, and that caspase-3 would be located furthest down stream of these apoptotic signals.

  • Research Products

    (8 results)

All Other

All Publications (8 results)

  • [Publications] Hamada Y: "Epairestat, an aldose reductase inhibitor, reduces the levels of N^ε-(carboxymethyl)lysine protein adducts and their precursors in erythrocytes from diabetic patients"Diabetes Care. 23. 1539-1544 (2000)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Naruse K: "Aldose reductase inhibition prevents glucose-induced apoptosis in cultured bovine retinal microvascular pericytes"Exp Eye Res.. 71. 309-315 (2000)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yasuda Y: "Role of PKC and TGF-β receptor in glucose-induced proliferation of smooth muscle cells"Biochem Biophys Res Commun.. 281. 71-77 (2001)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Nakamura J: "Glucose-induced hyperproliferation of cultured rat aortic smooth muscle cells through polyol pathway hyperactivity"Diabetologia. 44. 480-487 (2001)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Hatnada Y.: "Epalrestat; an aldose reductase inhibitor, reduces the levels of N'-(carboxymethyl)lysine protein adducts and their precursors in erythrocytes from diabetic patients"Diabetes Care. 23. 1539-1544 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Naruse K.: "Aldose reductase inhibition prevents glucose-induced apoptosis in cultured bovine retinal microvascular pericytes"Exp Eye Res. 71. 309-315 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yasuda Y.: "Role of PKC and TGF-/3receptor in glucose-induced proliferation of smooth muscle cells"Biochem Biophys Res Commun. 281. 71-77 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Nakamura J.: "Glucose-induced hyperproliteration of cultured rat aortic smooth muscle cells through polyol pathway hyperactivity"Diabetologia. 44. 480-487 (2001)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 2003-09-17  

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