| Project/Area Number |
13670456
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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 | Osaka University |
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Principal Investigator |
SAEKI Yukihiko Osaka University Graduate School Of Medicine Lecturer, 医学系研究科, 講師 (40240840)
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| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
|
| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Rheumatoid arthritis / NFIL-6 / Transcriptional factor / Knock out mouse / 慢性関節リウマチ / NFIL-6 / COX |
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| Research Abstract |
Previously, we demonstrated that the decoy for NFIL-6 inhibited COX2mRNA expression significantly (about 30%) in vitro on cultured synovial cells from the patients with RA. In the present study, to examine whether blockade of NFIL-6 signals could ameliorate arthritis, a histopathological comparative study was performed between OPN-/-mice and their wild type littermates induced with a murine arthritis model, AIA (antigen-induced arthritis). As a result, the severity of AIA on OPN-/-mice was significantly less compared with that of their wild type littermates (mean score of histopathological severity; OPN-/-versus wild type: 1.94±1.06 versus 2.78±0.73, p<0.05). These result suggest that NFIL-6 may be a possible therapeutic target for RA.
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