| Project/Area Number |
05670178
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Human pathology
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| Research Institution | Nagoya City University |
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Principal Investigator |
TADA Toyohiro Nagoya City University Medical School, Department of Pathology, Associate Professor, 医学部, 助教授 (20106230)
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| Co-Investigator(Kenkyū-buntansha) |
KUNIMATSU Mitoshi Nagoya City University Medical School, Depertment of Biochemistry, Assistant Pro, 医学部, 講師 (70145746)
OKADA Hidechika Nagoya City University Medical School, Institute for Molecular Biology, Professo, 医学部, 教授 (30160683)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | complement / myocardial infarction / cell death / ischemia / membrane attack complex / inflammation / cardiomyocyte / 補体制御因子 / DAF / HRF20 / 心臓 |
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| Research Abstract |
Loss of 20 KD homologous restriction factor of complement (HRF20)(CD59) from the cardiomyocytes in the area of myocardial infarction of human hearts was immunohistochemically demonstrated using monoclonal antibody 1F5. Complements deposition including membrane attack complex (MAC) was also immunohistochemically shown on the dead cardiomyocytes in the same (infarcted) area absent from HRF20. In patients of myocardial infarction of 4 hours or less than it of age, neither loss of HRF20 nor complements deposition was found in the myocardium. However, in cases of myocardial infarction of 21 hours or more than it of age, the dead cardiomyocytes in the infarcted area showed MAC deposition and complete loss of HRF20. Decay accelerating factor (DAF)(CD55) was also lost from the infarcted area by the same manner with HRF20. Outside the infarcted area, expression of HRF20 and DAF on the cardiomyocytes outside were well preserved without MAC deposition. Immunoglobulins, especially IgM,were also stained in the dead myocytes in the infarcted area, but no suggestion for its pathological significance and mechanism of deposition were given. Degradation of membrane structure of dead cardiomyocytes would cause removal of HRF20 from infarcted area. The present study suggested that loss of HRF20 from dead cardiomyocytes playd an important role to induce deposition of MAC in the infarcted area.
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