| Project/Area Number |
23591440
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
|
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| Research Institution | Hiroshima University (2012-2013)
Nagasaki University (2011) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SUGIYAMA Eiji 広島大学, 病院, 教授 (70179167)
KAWAKAMI Atsushi 長崎大学, 医歯(薬)学総合研究科, 教授 (90325639)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | リウマチ学 / マイクロRNA / 関節リウマチ / 滑膜細胞 / TGF / miRNA / 分化誘導 / 翻訳制御 / locked nucleic acid / サイトカイン / mRNA崩壊 / 受容体 |
|---|
| Research Abstract |
We identified miRNAs, which are induced in fibroblastic synovial cell from a patients with rheumatoid arthritis by treatment with TGFbeta1, a cytokine produced from immune cells. One of the miRNAs targets a transcript of secrete protein, which can be secreted form fibroblastic synovial cell. This implies that a miRNA induced by TGFbeta1 can reduce the secreted protein expression in rheumatoid arthritis. Since the secreted protein is involved in osteoblastgenic process, the miRNA is thought to contribute to osteoblast function in the disease. Namely, a method that regulate this miRNA may leads to enhancement of the bone regeneration process in destructed articular bone in rheumatoid arthritis.
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