| Project/Area Number |
07670236
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Niigata University School of Medicine |
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Principal Investigator |
MORIOKA Tetsuo NIIGATA UNIVERSITY SCHOOL OF MEDICINE Dept.Cellular Physiology Associate Professor, 医学部, 助教授 (00210146)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Fujio NIIGATA UNIVERSITY SCHOOL OF MEDICINE Dept.Cell Biology Professor, 医学部, 教授 (40012728)
OITE Takashi NIIGATA UNIVERSITY SCHOOL OF MEDICINE Dept.Cellular Physiology Professor, 医学部, 教授 (60018744)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | lupus nephritis / nucleosome / amyloid P component / histones / DNA / immune complexes / SLE / glomerular basement membrane (GBM) / 血清アミロイドP蛋白 |
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| Research Abstract |
With aid of the above grant, we have researched and reported on the mechanism of initiation of lupus nephritis. We have obtained the following results during the period of research project :
(1) Antibodies from serum of SLE patients can form soluble histone-DNA-anti-DNA immune complexes that bind to the glomerular capillary wall in vivo.
(2) Amyloid P component is a constituent of normal human glomerular basement membrane
(3) DNA and nucleosome core particles could bind to human GBM in the presence of Ca^<++.>
(4) Treatment of GBM with trypsin resulted the loss of amyloid P component on the GBM.The binding of DNA and nucleosome core particles to the GBM were reduced when GBM were treated with trypsin.
These results suggested that DNA and nucleosome core particles could bind to human GBM and this may cause the initiation of lupus nephritis.
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