| Project/Area Number |
19591749
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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 |
Orthopaedic surgery
|
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
HIRANO Fuminori Asahikawa Medical College, 医学部, 講師 (60250552)
|
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| Co-Investigator(Kenkyū-buntansha) |
MAKINO Yuichi 旭川医科大学, 医学部, 講師 (90345033)
OKAMOTO Kensaku 旭川医科大学, 医学部, 助教 (80396879)
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| Project Period (FY) |
2007 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2007: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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|---|
| Keywords | リウマチ病学 / 関節リウマチ / 滑膜炎 / 転写因子 / NF-κB / シグナル伝達 / 免疫学 / 核酸 / 臨床 / 発現制御 |
|---|
| Research Abstract |
Rheumatoid arthritis (RA) is an autoimmune disease to cause joint and cartilage destructions by the inflammation of a sustained synovium. NF-κB is a transcription factor and plays a pivotal role in regulating synovitis in RA. In unstimulated cells, NF-κB binds to inhibitory molecules IκBs and exists in cytoplasm. Especially, IκBβ2 has the strongest inhibitory effect against NF-κB activation in IκBs. Therefore, in this study, we found abnormal expression of the IκBβ2 protein which could restrain NF-κB and elucidated that the abnormal expresion of the IκBβ2 protein was due to produce RNA-binding protein and microRNA expression. The new RA treatment of the few type may be developed conventionally in future by these results of research.
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