| Project/Area Number |
21592332
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
LI Yinji 九州大学, 歯学研究院, 助教 (90457424)
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| Co-Investigator(Kenkyū-buntansha) |
久木田 敏夫 (久木田 明子) 佐賀大学, 医学部, 准教授 (30153266)
久木田 敏夫 九州大学, 歯学研究院, 教授 (70150464)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 口腔解剖学(含組織学・発生学) / ガレクチン3 / 糖鎖結合ドメイン / N末端領域 / 破骨細胞分化 / タンデム型ガレクチン / 膜表面受容体 / 炎症性骨破壊 / 組み替え蛋白質 / 新規レセプター |
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| Research Abstract |
Galectin 3 is the factor which regulates inflammatory bone destruction and suppresses osteoclastogenesis. As the inhibitory activity of galectin 3 was not attributed to the carbohydrate recognition domain(CRD), N-terminal region was considered to have regulatory roles in the regulation of osteoclastogenesis. N-terminal region of galectin-3 was recloned and recombinant protein was obtained, however, we have failed in obtaining active recombinant polypeptides bearing inhibitory activity on osteoclastogenesis. We then examined other types of galectin. Galectin 9 is the tandem type of galectin with two CRDs connected by a linker polypeptide. Galectin 1 is the prototype galectin composed of only two CRD. Although galectin 1 did not affect osteoclastogenesis, galectin 9 markedly inhibited osteoclastogenesis in a dose-dependent manner. The inhibition of osteoclastogenesis by galectin 9 was partly canceled by the addition of lactose. It was strongly suggested the presence of CRD-dependent mechanism as well as CRD-independent mechanism. We further examined if the galectin 9 receptor is expressed in osteoclast precursors and found that some receptor molecules regulating apoptosis are expressed in osteoclast precursors. This research would provide important tool and strategy for controlling inflammatory bone destruction.
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