1989 Fiscal Year Final Research Report Summary
Mechanisms of cell proliferation and extracellular matrix production in glomeruli
| Project/Area Number |
63570155
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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 |
Experimental pathology
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| Research Institution | Niigata University School of Medicine |
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Principal Investigator |
OITE Takashi Niigata University School of Medicine, Inst. of Nephrology, Dept. of Immunology, Associate Professor, 医学部, 助教授 (60018744)
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| Co-Investigator(Kenkyū-buntansha) |
ORIKASA Michiaki Niigata University School of Dentistry, Dept. of Pharmacology, Assistant, 歯学部, 助手 (30185681)
YOSHIDA Kazukiyo Niigata University School of Medicine, Dept. of Internal, Medicine Assistant, 医学部, 助手 (70174919)
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| Project Period (FY) |
1988 – 1989
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| Keywords | RENAL GLOMERULI / GLOMERULAR SCLEROSIS / EXTRACELLULAR MATRIX / CELL PROLIFERATION / EXPERIMENTAL NEPHRITIS / CULTURE OF GLOMERULI / GROWTH FACTORS / HAPTEN-SPECIFIC INJURY |
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| Research Abstract |
With aid of the above grant, we have researched and reported on the mechanisms of cell proliferation and extracellular matrix increment in the renal glomeruli. The following results have been obtained during the period of research project:
1).Monocyte-macrophage line cells were detected electron microscopically and immunohistologically within the inflamed glomeruli from human (using renal biopsy) and experimental animals.
2).Electrophoretic patterns of urinary proteins corresponded to differences in morphological expression such as proliferative changes in experimental glomerulonephritis (GN) models.
3).Using culture of isolated glomeruli, we found a human monocute-derived factors which were able to induce proliferation of glomerular mesangial cells in vitro. One of this factors is similar in nature to platelet- derived growth factor.
4).Furthermore, we detected the enhancing activity of extracelluar matrix production in the culture supernatant of human monocytes.
5).We reported a new model of experimental GN model in which marked exudative and proliferative changes in glomeruli and cellular influx containing Ia-positive leukocytes. Using this model of hapten-specific glomerular injury, mechanisms responsible for inducing cell infiltration and cell proliferation within glomeruli could be researched at molecular and cellular levels.
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