2020 Fiscal Year Annual Research Report
関節リウマチの骨破壊を誘導する滑膜線維芽細胞サブセットの同定
Project/Area Number |
19J21942
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Research Institution | The University of Tokyo |
Principal Investigator |
顔 明露 東京大学, 大学院医学系研究科, 特別研究員(DC1)
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Project Period (FY) |
2019-04-25 – 2022-03-31
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Keywords | Rheumatoid arthritis / Bone destruction / Synovial fibroblasts |
Outline of Annual Research Achievements |
Arthritic synovial fibroblasts were isolated from the arthritic joints, defined by the lack of CD45, CD31, CD146 expression, but surface protein podoplanin (gp38) expression. We used these surface protein antibodies to distinguish fibroblasts from the other cell populations in arthritic joints. Within the fibroblasts populations, we used a novel RANKL reporter mice to purified the osteoclastogenic fibroblasts which express RANKL. We next performed RNA-seq and epigenetic analysis to characterize the RANKL- expressing fibroblasts in both genomic and epigenetic levels.
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Current Status of Research Progress |
Current Status of Research Progress
1: Research has progressed more than it was originally planned.
Reason
今年度では滑膜線維芽細胞が骨破壊誘導能を獲得する機構をエピジェネティックレベ ルで解明することに成功しつつあり、その生体レベルで証明すべく精力的に研究を進めている。本領域は 関節リウマチの骨破壊を理解する上で非常に重要であり期待以上の研究の進展があったといえる。
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Strategy for Future Research Activity |
In the future, we will further explore the high-throughput sequencing data and find the candidate bone-destructive surface molecules. Genetically or pharmaceutically targeting these surface molecules will yield promising clinical benefits for treating joint destructive diseases.
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[Journal Article] Plasma cells promote osteoclastogenesis and periarticular bone loss in autoimmune arthritis2021
Author(s)
Noriko Komatsu, Stephanie Win, Minglu Yan, Nam Cong-Nhat Huynh, Shinichiro Sawa, Masayuki Tsukasaki, Asuka Terashima, Warunee Pluemsakunthai, George Kollias, Tomoki Nakashima, and Hiroshi Takayanagi
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Journal Title
J Clin Invest
Volume: 131(6)
Pages: e143060
DOI
Peer Reviewed / Open Access / Int'l Joint Research
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