| Project/Area Number |
10670990
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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 |
Kidney internal medicine
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
MARUYAMA Hiroki NIIGATA UNIVERSITY, NIIGATA UNIVERSITY MEDICAL HOSPITAL, Assistant, 医学部・附属病院, 助手 (10293218)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2000: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | transgenic mice / human β_2-microglobulin / CAG promoter / dialysis-related amyloidsis / 透析アミロイド-シス / CAGベクター |
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| Research Abstract |
To clarify the pathogenesis and establish therapy of dialysis-related amyloidosis, , we cloned humanβ_2-M cDNA by RT-PCR.We inserted humanβ_2-M cDNA into unique XhoI site of pCAGGS.We generated transgenic mice overexpressing humanβ_2-M (F0 5 lines). We confirmed humanβ_2-MmRNA by RT-PCR and northern blotting analysis, serum and urine humanβ_2-M by western blotting. We generated homozygote transgenic mice by mating F1. Serum humanβ_2-M levels (20-30mg/l)were as high as those levels in hemodialyzed patients. We could not observe dialysis-related amyloidosis in transgenic mice. These results demonstrated that only hyper β_2-M could not cause dialysis-related amyloidosis. We observe dialysis-related amyloidosis patients with chronic renal failure. To add a crucial factor, chronic renal failure, for development of dialysisrelated amyloidosis, we created five-sixths nephrectomized transgenic mice. We will analyze these mice.
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