Mechanism of bone and cartilage deterioration in rheumatoid arthritis via RANKL/Fas signaling
Project/Area Number |
23659966
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Orthodontic/Pediatric dentistry
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Research Institution | The University of Tokushima |
Principal Investigator |
TANAKA Eiji 徳島大学, 大学院・へルスバイオサイエンス研究部, 教授 (40273693)
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Co-Investigator(Kenkyū-buntansha) |
KURODA Shingo 徳島大学, 大学院・へルスバイオサイエンス研究部, 准教授 (40332796)
HIASA Masahiro 徳島大学, 大学院・へルスバイオサイエンス研究部, 助教 (90511337)
FUJIHARA Shinji 徳島大学, 病院, 助教 (70403706)
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Project Period (FY) |
2011 – 2012
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Project Status |
Completed (Fiscal Year 2012)
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Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
Keywords | 歯科矯正学 / 関節リウマチ / RANKLシグナル / 破骨細胞 / 免疫細胞 / 関節骨破壊 / 樹状細胞 |
Research Abstract |
In this study, we investigated the functions of osteoclasts (Ocs) from MRL/lpr mice, animal model for human rheumatoid arthritis (RA), bearinf a mutant of Fas gene. In vitro and in vivo experiments showed enhanced function of MRL/lpr Ocs as antigen-presenting cells to activate peripheral T cells. Furthermore, the migratory response of MRL/lpr Ocs to S1P was significantly enhanced. The hyperfunctions of Ocs in MRL/lpr mice play a potent role in the pathogenesis for RA with bone destruction. Fas signaling of Ocs may regulate the differentiation, activation, and migration of Ocs.
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Report
(3 results)
Research Products
(15 results)
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[Journal Article] Fas-Independent T-Cell Apoptosis by Dendritic Cells Controls Autoimmune Arthritis in MRL/lpr Mice2012
Author(s)
Takashi Izawa, Tomoyuki Kondo, Mie Kurosawa, Ritsuko Oura, Kazuma Matsumoto, Eiji Tanaka, Akiko Yamada, Rieko Arakaki, Yasusei Kudo, Yoshio Hayashi and Naozumi Ishimaru
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Journal Title
PLoS ONE
Volume: Vol.7, No.12
Issue: 12
Pages: e48798-e48798
DOI
NAID
Related Report
Peer Reviewed
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