| Project/Area Number |
20592173
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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 |
Functional basic dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
NISHIDA Takashi Okayama University, 大学院・医歯薬学総合研究科, 助教 (30322233)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIGAWA Masaharu 岡山大学, 大学院・医歯薬学総合研究科, 教授 (20112063)
KUBOTA Satoshi 岡山大学, 大学院・医歯薬学総合研究科, 准教授 (90221936)
HATTORI Takako 岡山大学, 大学院・医歯薬学総合研究科, 助教 (00228488)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | CCN2 / CTGF / 破骨細胞形成 / GST-RANKL / CCN2欠損マウス / 骨吸収活性 / fetal liver cells / DC-STAMP / retrovirus / CCN2/CTGF / CCN2産生過剰マウス / fetal liver cell / RANKL / TRAP染色 / CTGF欠損マウス / M-CSF / 内軟骨性骨化 / RAW264.7細胞 |
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| Research Abstract |
Combination of RANKL, M-CSF and CCN2 significantly enhanced tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cell formation compared with RANKL and M-CSF. Therefore, we suspected the involvement of CCN2 in cell-cell fusion during osteoclastogenesis. To clarify the mechanism, we isolated fetal liver cells from Ccn2-null mice at E14.5 days, and investigated TRAP-positive multinucleated cell formation. The results showed that RANKL-induced osteoclastogenesis was impaired in fetal liver cells from Ccn2-null mice, and the impaired osteoclast formation was rescued by the addition of exogenous CCN2. These results suggest that CCN2 involves in cell-cell fusion during osteoclastogenesis.
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