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ISOLATION AND CHARACTERIZATION OF CYTOKINES SECRETED FROM CARDIAC MYXOMAS AND APPLICATION FOR CONGESTIVE HEART FAILURE

Research Project

Project/Area Number 07670752
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionGUNMA UNIVERSITY

Principal Investigator

KANDA Tsugiyasu  GUNMA UNIVERSITY SCHOOL FROM MEDICINE,DEPARTMENT OF LABORATORY MEDICINE,INSTRUCTOR., 医学部, 助手 (40261838)

Co-Investigator(Kenkyū-buntansha) KOBAYASHI Isao  GUNMA UNIVERSITY SCHOOL OF MEDICINE,DEPARTMENT OF LABORATORY MEDICENE,PROFESSOR., 医学部, 教授 (50008273)
Project Period (FY) 1995 – 1996
Project Status Completed (Fiscal Year 1996)
Budget Amount *help
¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Keywordsinterleukin-6 / interleukin-8 / cardiac myxoma / myocarditis / ウイルス / インターロンキン-6 / インターロンキン-8 / ウイルス性心筋炎 / 心不全
Research Abstract

We investigated the structure and charactrization of cytokines secreted from cardiac myxomas and analyzed the role of these cytokines for cangestive heart failure. Among eighteen cases of cardiac myxomas, 15 cases (83%) wass positively stained with antiinterleukin-6 (IL-6) antibody. Patients with IL-6 positive cardiac myxomas showed autoimmune like symptoms, such as weghtoloss, easy fatigability and fever. Their laboratory findings revealed higher levels of immunoglobulin G and A or gamma-globulin. Cytokines secreted from cardiac myxoma was analyzed by Western blotting. The molecular weight was about 10 to 12 kDa. This band was positive with anti-interleukin-8 (IL-8) antibodies.
Cultured supernatants obtained from cardiac myxomas inproved the survival of mice infected with encephalomyocarditis virus (EMCV). We compared the effects for viral myocarditis inbetween IL-6 and IL-8. IL-6, not IL-8, was beneficial for viral myocarditis of mice. Histopathological examination and viral analysis showed the reduction of myocarial necrosis by IL-6.
Therefore, we hypohtesize that IL-6 secreted from cardiac myxoma induces autoimmune like symptoms in patients with cardiac myxoma and that IL-6 is beneficial for the reduction of cardiac myxomas of mice induced from EMCV.

Report

(3 results)
  • 1996 Annual Research Report   Final Research Report Summary
  • 1995 Annual Research Report
  • Research Products

    (7 results)

All Other

All Publications (7 results)

  • [Publications] 神田享勉他: "Modification of viralmyocarditis by interleukin-6" Circ.Res.78・5. 848-856 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] 神田享勉他: "Interleukin-6 secreted from human myxoma reduces murine myocarditis" Life Sci.58・20. (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] 神田享勉他: "Interleukin-6 secreted from human myxoma reduces murine myocarditis" Life Sci.58・20. (1996)1705-1712

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Kanda-T,McManus-JW,Imai-S,Decheng Yang, McManus-BM,Suzuki-T,Nagai-R,Kobayashi-I.: "Modification of viral myocarditis by interleukin-6" Circ-Res. 78. 848-856 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Kanda-T,Sakamoto-H,McManus-BM,Sakamaki-T,Suzuki-T,Nagai-R,Kobayashi-I.: "Interleukin-6 secreted from human myxoma reduces murine viral myocarditis." Life-Sci. 58. 1705-1712 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] 神田享勉 他: "Modification of viralmyocarditis by interleukin-6" Circ.Res.78・5. 848-856 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] 神田享勉 他: "Interlenkin-6 secreted from human myxomn reduces murin myocodies" Life Sci.58・20. 1705-1712 (1996)

    • Related Report
      1996 Annual Research Report

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Published: 1996-04-01   Modified: 2016-04-21  

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