1993 Fiscal Year Final Research Report Summary
Mechanisms of sclerosis in the glomerulus as a representative of microcirculation
| Project/Area Number |
04670199
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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 |
作物
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| Research Institution | Niigata University |
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Principal Investigator |
OITE Takashi Niigata University School of Medicine Dept. of Immunology Associate Professor, 医学部, 助教授 (60018744)
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| Co-Investigator(Kenkyū-buntansha) |
MORIOKA Tetsuo Niigata University School of Medicine Dept. of Immunology Assistant, 医学部, 助手 (00210146)
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| Project Period (FY) |
1992 – 1993
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| Keywords | glomerulus / microcirculation / endothelial cells / mesangial cells / sclerotic lesions / cell proliferation / extracellular matrix / TGF-beta |
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| Research Abstract |
With aid of the above grant, we have researched and reported on the mechanisums of glomerulosclerosis. We have obtained the following results during the period of research project :
(1) When human mesangial cells(HMC) were cultured on a reconstituted basement membrane, Matrigel HMC aggregated and formed isolated colonies, then extended an array of cell processes to form a dendritic network structure and proliferated very slowly. On type I collagen gel, HMC showed rapid cell growth.
(2) Mesangial cell proliferation was inhibited markedly on gels containing type III collagen, heparin and heparan sulphate ; type IV collagen suppressed HMC proliferation.
(3) Conditioned medium(CM) of cultured mesangial cells showed the inhibitory activity on mesangial cell proliferation, which was absorbed with anti-TGF-beta antibody. In CM, less than 10% of TGF-beta was present in active form. Direct addition of anti-TGF-beta antibody to culture media enhanced mesangial cell proliferation.
(4) The effect of direct cell contact between endothelial and mesangial cells on mesangial cell behavior was examined in a coculture system. MoAb.1-22-3 was bound preferentially to the limited mesangial cell surface facing endothelial cells.
(5) There is a difference in reactivity between MoAb.1-22-3 and anti-Thy1.1 Ab(OX-7).
Now, we are investigating a new epitope detected with MoAb.1-22-3 at the cellular (immune electronmicroscopic) and molecular (using cDNA for Thy-1 gene) levels.
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