| Project/Area Number |
25670780
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
KUKITA Toshio 九州大学, 歯学研究科(研究院), 教授 (70150464)
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| Co-Investigator(Kenkyū-buntansha) |
久木田 明子 佐賀大学, 医学部, 准教授 (30153266)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | 炎症性骨破壊 / 免疫制御 / アジュバント関節炎 / Tim-3 / ガレクチン９ / 破骨細胞 / ガレクチン9 / Th1細胞 |
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| Outline of Final Research Achievements |
The purpose of this study is to analyze the expressional change of the Tim-3 and its ligand galectin-9 in the process of inflammatory bone destruction. In normal rats, Tim-3 expression was well consistent with the location of osteoclasts and their mononuclear precursors. Expression of Tim-3 ligand galectin-9 was detected in the bone marrow periphery facing to the bone surface. In contrast, expression of Tim-3 and its ligand galectin-9 was detected in whole areas of marrow cavity. To know the function of Tim-3 in osteoclastogenesis, galectin-9 was added to the cultures of evaluating osteoclast differntiation in vitro. Galectin-9, markedly inhibited osteoclastogenesis. When galectin-9 was injected around the ankle joint of the rats with adjuvant-induced arthritis, inflammatory bone destruction was marketly suppressed. This research shows the possibility of developing a novel therapy using an new regulatory system of Tim-3/galectin-9.
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