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Autoantibody against muscarininc acetylcholine Receptor as a possible cause of Raynauds'phenomenon.

Research Project

Project/Area Number 62570372
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Neurology
Research InstitutionFujita-Gakuen Health University

Principal Investigator

TORIKAI Katsutaka  Professor, Dept. of Internal Medicine, School of Medicine., 医学部 内科学, 教授 (50084520)

Co-Investigator(Kenkyū-buntansha) NAGATA Yutaka  Professor, Dept, of Physiology, School of Medicine., 医学部 生理学, 教授 (70084499)
INADA Shinichi  Assistant Professor, Dept. of Internal Medicine, School of Medicine., 医学部 内科学, 講師 (70129336)
YOSHIDA Syunji  Associate, Dept. of Internal Medicine, School of Medicine., 医学部 内科学, 助手 (00166951)
Project Period (FY) 1987 – 1988
Project Status Completed (Fiscal Year 1988)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,900,000 (Direct Cost: ¥1,900,000)
KeywordsRaynaud's phenomenon / Collagen Disease / Autoantibody / Arterial Relaxing Faotor / Acetycholine Receptor / 血管内皮 / レイノー現象 / ムスカリン性アセチルコリン受容体
Research Abstract

We tried to unlock the mechanism of the occurrence of Raynaud's phenomenon in collagen diseases. Due to the presence of auto-antibodies to muscarinic acetylcholine receptor (m-AchR), hypofunction of m-AchR at the vascular level could occur, and this would be responsible for hindering the inhibition of angiospasm. We therefore studied the possibilities of the development of Raynaud's phenomenon. At the beginning, we determined antibodies using m-AchR extracted from a human brain as an antigen, with the result that we identified a factor inhibiting m-AchR in serum IiG in collagendisease patients with Raynaud's phenomenon. Taking notice of report stating that EDRF (vascular relaxation factor) is secreted from angio-endothelial cells, we also considered the possibilities of a lowering of EDRF levels due to the cytotoxic activity of the patient's serum for endothelial cells. The result was that rate of "dead cells" (this was determined by the dye exclusion method), which was used to indicate the impeding activity of the patient's whole serum for endothelial cells, was significantly higher in both Raynaud's phenomenon positivity and vasculitis complication groups than in healthy volunteers as controls. The patient's serum gamma-globulin and IgG fractions were then purified and examined, with the result that the rate of "dead cells" was higher in the Raynaud's phenomenen positivity group than in the control group. These results suggested that the development of Raynaud's symptoms may be associated not only with auto-antibodies to m-AchR but also with impediment of EDRF which is reportedly secreted from vascular endothelial cells.

Report

(3 results)
  • 1988 Annual Research Report   Final Research Report Summary
  • 1987 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] 加藤真知子、吉田俊治、鳥飼勝隆、永田豊: 藤田学園医学会誌. 11 (2). 347-350 (1987)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1988 Final Research Report Summary
  • [Publications] 加藤満知子: 藤田学園医学会誌.

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1988 Final Research Report Summary
  • [Publications] Machiko Kato; Shunji Yoshida; Katsutaka Torikai; Yutaka Nagata.: "Cytotoxic factor against angio-endothelial cells in connective tissue diseases." Bulletin of the Fujita-Gakuen Medical Society. 11(2). 347-350 (1987)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1988 Final Research Report Summary
  • [Publications] Machiko Kato.: "Study on the pathogenesis of Raynaud's phenomenon." Bulletin of the Fujita-Gakuen Medical Society. (1989)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1988 Final Research Report Summary
  • [Publications] 加藤真知子.鳥飼勝隆: 藤田学園医学会誌. 13. (1989)

    • Related Report
      1988 Annual Research Report
  • [Publications] 加藤 眞知子: 藤田学園医学会誌. (1988)

    • Related Report
      1987 Annual Research Report

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Published: 1987-04-01   Modified: 2016-04-21  

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