| Project/Area Number |
21390492
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 |
KUKITA Toshio 九州大学, 歯学研究院, 教授 (70150464)
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| Co-Investigator(Kenkyū-buntansha) |
KUKITA Akiko 佐賀大学, 医学部, 准教授 (30153266)
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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 |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2009: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
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| Keywords | 口腔解剖学 / 含組織学・発生学 / 間葉系幹細胞 / 表面マーカー / モノクローナル抗体 / 細胞分化 / 骨髄 / 膜表面抗原 / 病的骨吸収 / 免疫抑制 |
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| Research Abstract |
The purpose of this research is to develop the cell-surface marker of mesenchymal stem cells(MSCs) and to regulate inflammatory bone destruction of animals bearing arthritis. As the isolation of mouse MSCs had problem in its purity and reproducibility in purification, we have focused on isolating and applying rat MSCs on the development of cell surface markers for MSC and regulation of inflammatory bone destruction on adjuvant-induced arthritis in rats. Isolated rat MSCs in the presence of basic FGF differentiated into osteoblasts, chondrocytes and adipocytes and expressed surface phenotypes of CD90+, CD29+, CD31-, CD45-. MSCs significantly inhibited osteoclastogenesis. MSCs expressed OPG and IL10, cytokines suppressing osteoclastogenesis, and chemokine receptors CCR1, CCR3 and CXCR4. MSCs had migratory activity against MIP-1αand SDF-1α, chemokines expressed in the area of inflammatory bone destruction. MSCs injected to rats with adjuvant-induced arthritis markedly suppressed inflammatory bone destruction. It was suggested that administrated MNCs migrate to the site of inflammatory bone destruction and suppress osteoclastogenesis.
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