| Project/Area Number |
10670743
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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 | Fukushima Medical University School of Medicine |
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Principal Investigator |
SUZUKI Hitoshi Fukushima Medical University School of Medicine, Pediatrics, Professor, 医学部, 教授 (80045682)
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| Co-Investigator(Kenkyū-buntansha) |
KAWASAKI Yukihiko Fukushima Medical University School of Medicine, Pediatrics, Research Associate, 医学部, 助手 (00305369)
SUZUKI Shigeo Fukushima Medical University School of Medicine, Pediatrics, Research Associate, 医学部, 助手 (00274960)
SUZUKI Junzo Fukushima Medical University School of Medicine, Pediatrics, Associate Professor, 医学部, 助教授 (20171217)
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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 |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Experimental IgA nephropathy / Coxsackievirus B4 / CAR / Adenovirus / Viral receptor |
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| Research Abstract |
We have been reporting that the mice injected coxsackievirus intravenously affect the mesangial proliferative glomerulonephritis similar to IgA-nephropathy. On the other hand, the ability of viruses to infect host cells is dependent on the presence of an appropriate cellular receptor. Recently, adenoviruses and coxsackievirus share one common receptor, and the receptor has been identified as a common coxsackievirus and adenovirus receptor ; CAR.The distribution of CAR may influence the pathophysiology of virus induced glomerulonephritis.
Therefore, we examined the expression of CAR in various organs of adult rat and mouse. The results were as follows ;
1) The expression of CAR was detected in almost all organs of mouse or rat.
2) CAR messages were detected stronger in the digestive-system internal organs, such as digestive tract and liver.
3) CAR messages were also detected in the kidney, especially in the renal-cortex part.
4) In the model of nephrotic syndrome, the expression of CAR messages in rat kidneys was enhanced during the early stages of the illness.
In conclusion, the above results indicate that coxsackievirus may serve as the initiated factors of renal disease.
Furthermore, in patients involved various glomerulonephritis or nephrotic syndrome, the disease may be highly influenced by viral infections and the viral infections may cause the acute aggravation of the renal disease or relapse.
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