Identification and analysis of chondroitin sulfates which regulate bone remodeling, and control of bone mass
| Project/Area Number |
23780293
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Tottori University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 破骨細胞 / 骨芽細胞 / コンドロイチン硫酸 / 骨リモデリング / 分化 / RANKL / RANK / 骨吸収能 / 骨形成と骨分解 / 骨粗鬆症 / OVXマウス / M-CSF / 水晶電子マイクロバランス法 / 細胞の分化 / CS-E / CS-0 / ハウシップ窩 |
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| Research Abstract |
In present study, I investigated the osteoclast inhibition ability in CS and the mechanism how CS inhibit osteoclast differentiation in vitro. CS was significantly inhibited the number of tartrate-resistance acid phosphatase (TRAP)-positive multinucleated cells and bone resorption activity in pit formation assay.In quartz-crystal microbalance method, CS revealed the binding ability to RANKL and interrupted binding of RANK to RANKL. Furthermore, CS reduced the phosphorylation of extracellular ERK in pre-osteoclast cells. These results indicate that CS suppress osteoclast size and osteoclastogenesis by binding to RANKL and inhibited RANK signal pathway.
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Report
(4 results)
Research Products
(11 results)
