2001 Fiscal Year Final Research Report Summary
Analysys of upregulated gene expression of interleukin-15 by synoviocytes in patients with rheumatoid arthritis
| Project/Area Number |
12670411
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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 | HOKKAIDO UNIVERSITY |
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Principal Investigator |
AMASAKI Yoshiharu Hokkaido Univ., Grad. School of Medicine, Research Assistant, 医学部・附属病院, 助手 (50312369)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Interleukin-15 / TNFα / transctiption factor / Rheumatoid arthritis / synoviocytes / macrophages |
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| Research Abstract |
TNFα-TNF receptor signaling is known to play a pivotal role in the promotion of joint destruction in Rheumatoid arthritis (RA). It has been recently reported that Interleukin-15 (IL-15) a newly discovered cytokine largely produced by macrophages, is increased in synovial fluid in RA, and can mediate secretion of TNFα. In current study, upregulated mRNA expression of IL-15 in rheumatoid synoviocytes was investigated by using freshly isolated and cultured synoviocytes from RA or osteoarthritis (OA) patients. mRNA expression analyzes using RT-PCR showed upregulated expression of IL-15 by synoviocytes, not only from RA patients but also from some OA patients. Expression of IL-15 was also observed in both RA and OA synoviocytes at protein levels by using intracellular FACS staining, indicating that IL-15 expression by itself is not specific to RA. When stimulated by TNFα or LPS, both RA and OA synoviocytes showed stimulation dependent upregulation of IL-15 mRNA. Since NF-κB and IRF-1 have been shown to be critical transcription factors in IL-15 mRNA regulation, EMSA analysis using these cis-acting elements from IL-15 promoters was also performed. Upon stimulation by either of TNFα or LPS, increased NF-κB DNA-binding activity was induced while not in IRF-1 DNA-binding. These results suggest that IL15 is not RA-specific inducer of TNFα expression, but enhancer of TNFα gene expression that mutually act through induction of NF-κB activities.
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Research Products
(10 results)
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[Publications] ENDO, T, ODA, A., SATOH, I., HASEYAMA, Y, NISHIO, M., KOIZUMI, K, TAKASHIMA, H., FUJIMOTO, K., AMASAKI, Y., FUJITA, H., KOIKE, T., SAWADA, K.: "Stem cell factor protects c-kit+ human primary erythroid cells from apoptosis"Exp Hematol. 29. 833-841 (2001)
Description
「研究成果報告書概要(和文)」より
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[Publications] ENDO, T., ODA, A., SATOH, I., HASEYAMA, Y., NISHIO, M., KOIZUMI, K, TAKASHIMA, H., FUJIMOTO, K., AMASAKI. Y., FUJITA, H., KOIKE, T., SAWADA, K.: "Stem cell factor protects c-kit+ human primary erythroid cells from apoptosis."Exp Hematol. 29. 833-41 (2001)
Description
「研究成果報告書概要(欧文)」より
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