2015 Fiscal Year Final Research Report
Study of the role of miRNA in the regulation of osteoclast differentiation in rheunmatoid arthritis joints
Project/Area Number |
25461476
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Collagenous pathology/Allergology
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Research Institution | Kobe University |
Principal Investigator |
Kawano Seiji 神戸大学, 医学部附属病院, 教授 (20351512)
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Co-Investigator(Kenkyū-buntansha) |
SAEGUSA Jun 神戸大学, 医学部附属病院, 講師 (20514970)
NAKAMACHI Yuji 神戸大学, 医学部附属病院, その他(臨床検査技師) (80379429)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | マイクロRNA / 破骨細胞 / 関節リウマチ |
Outline of Final Research Achievements |
MicroRNAs (miRNAs) are small endogenous, noncoding RNAs that act as post-transcriptional regulators. We analyzed the in vivo effect of miRNA-124 (miR-124, the rat analog of human miR-124a) on adjuvant-induced arthritis (AIA) in rats. We found that miR-124 suppressed AIA in rats, as demonstrated by decreased synoviocyte proliferation, leukocyte infiltration, and cartilage or bone destruction. Osteoclast counts were reduced in AIA rats treated with pre-miR-124, and protein level of NFATc1 was reduced in AIA joints. Luciferase analysis showed that miR-124 directly targeted the 3’-UTR of the rat NFATc1 mRNAs. MiR-124 also directly targeted the 3’-UTR of human NFATc1 mRNA, and suppressed the differentiation of human osteoclasts.Conclusion. We found that miR-124 ameliorated AIA by suppressing critical prerequisites for arthritis development, such as NFATc1. Thus, we concluded that miR-124a is a candidate for therapeutic use for human rheumatoid arthritis.
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Free Research Field |
リウマチ膠原病学
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