| Project/Area Number |
25462888
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
Hattori Takako 岡山大学, 医歯(薬)学総合研究科, 助教 (00228488)
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| Co-Investigator(Kenkyū-buntansha) |
KUBOTA Satoshi 岡山大学, 大学院医歯薬学総合研究科, 教授 (90221936)
NISHIDA Takashi 岡山大学, 大学院医歯薬学総合研究科, 准教授 (30322233)
TAKIGAWA Masahasu 岡山大学, 大学院医歯薬学総合研究科, 教授 (20112063)
AOYAMA Eriko 岡山大学, 大学院医歯薬学総合研究科, 助教 (10432650)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | NOV/CCN3 / トランスジェニックマウス / 内軟骨性骨形成 / in situ hybridization / 間葉系細胞 / 軟骨分化 / 高密度培養系 / SFRP5 / 関節変性 / 血管侵入 / Col2a1 promoter |
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| Outline of Final Research Achievements |
To understand a role of CCN3 in bone formation, we generated a transgenic mouse line which is specifically overexpressing CCN3 in cartilage. The mice showed embryonic bone malformations, including shortened long bones, decreased bone mineralization, and delayed appearance of osteoblasts and cells expressing marker genes of late hypertrophy. Blood vessel invasion into the developing cartilage was also inhibited. In contrast, limb mesenchymal cells showed accelerated chondrogenesis. These phenomena correlated with changes in gene expression related to bone and cartilage development. Moreover, we observed degradation of articular chondrocytes and absorption of subchondral bone in adult knee joints. These findings demonstrate a novel role of CCN3 in skeletal development and maintenance of articular cartilage.
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