| Project/Area Number |
11670452
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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 |
内科学一般
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| Research Institution | Nagasaki University |
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Principal Investigator |
MIGITA Kiyoshi Nagasaki University School of Medicine, First Department of Internal Medicine, Assistant Professor, 医学部・附属病院, 講師 (60264214)
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| Co-Investigator(Kenkyū-buntansha) |
EGUCHI Katsumi Nagasaki University School of Medicine, First Department of Internal Medicine, Professor, 医学部, 教授 (30128160)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Serum amyloid A protein / β2-microglobulin / amyloidosis / cyclooxygenase-2 / cytokine / Rhumatoid arthritis / IL-18 / 単球 / シクロオキシゲナーゼ |
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| Research Abstract |
#1 Induction of COX-2 by β2-microglobulin
β2-microglobulin treatment increased the induction of COX-2 mRNA and COX-2 protein synthesis from human rheumatoid synovial cells in a dose-dependent manner. Dexamethasone suppressed the induction of COX-2 mRNA and protein in β2-microglobulin-stimulated synovial cells. These data indicated that COX-2 expression by β2-micoglobulin may be an important inflammatory process in hemodialysis associated osteoaithropathy.
#2 Impaired degradation of serum amyloid A protein by cytokine-stimulated monocytes.
CD14+ monocytes degraded SAA completely in vitro. When CD14* monocytes were pretreated with IL-1 β or IFN-γ, increasing amounts of SAA-related derivatives were detected in culture supernatants. This down-regulated proteolysis of SAA protein by cytokine stimulated monocytes may play a role in the mechanism of impaired SAA metabolism.
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