| Project/Area Number |
08670894
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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 |
Pediatrics
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KAGAMI Shoji SCHOOL OF MEDICINE,The University of Tokushima ASSISTANT PROFESSOR, 医学部, 講師 (00224337)
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| Co-Investigator(Kenkyū-buntansha) |
KIDO Hiroshi INSTITUTE OF ENZYME RESEARCH,The University of Tokushima PROFESSOR, 酵素科学研究センター, 教授 (50144978)
KURODA Yasuhiro SCHOOL OF MEDICINE,The University of Tokushima PROFESSOR, 医学部, 教授 (20035471)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1996: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | monoclonal antibody / 1F3 / Integrin / progression factors in GN |
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| Research Abstract |
In order to identify a new cell surface antigen as a potential marker of renal glomerular cell injury, we produced a monoclonal antibody (Mab), 1F3, by immunizing mice with cultured human glomerular cells. Immunohistochemical studies demonstraated that 1F3 recognizing molecule (1F3 molecule) was strongly expressed on the cell surface of glomerular podocytes and very weakly on parietal epithelial cells in the normal kidney. Immunoprecipitation revealed that 1F3 recognized a 125 KDa protein under reducing conditions. Sequenced N-terminal amino acid analysis following 1F3 immunoaffinity purification indicated that 1F3 molecule resembled integrin alpha3 subunit. Biopsy specimens from patients with a variety of glomerular and tubulointerstitial diseases showed that 1F3 antigen was almost negative in cellular crescents but was strongly expressed in fibro-cellular crescents. 1F3 antigen became positive in atrophic tubules that were seen in diseased kidneys. Severity of tubular atrophy correlated well with the extent of tubular expression of 1F3 antigen. Urine examination using ELISA showed that increased excretion of 1F3 molecule was observed in the patients with glomerulonephritis as compared with healthy donor. These results indicate that Mab, 1F3 marks cell biological changes of renal epithelial cells under disease conditions and may be a useful marker for progressive kidney diseases.
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