| Project/Area Number |
18K09503
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Review Section |
Basic Section 57010:Oral biological science-related
|
|---|
| Research Institution | Tokyo Medical and Dental University |
|---|
Principal Investigator |
Nakahama Ken-ichi 東京医科歯科大学, 大学院医歯学総合研究科, 准教授 (60281515)
|
|---|
| Project Period (FY) |
2018-04-01 – 2021-03-31
|
| Project Status |
Completed (Fiscal Year 2020)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
|
|---|
| Keywords | 破骨細胞 / 間葉系幹細胞 / 遊走因子 / 骨リモデリング / 骨芽細胞 |
|---|
| Outline of Final Research Achievements |
Bone is always renewed by new bone forming cells after bone resorption. It is not known the mechanism by which the bone forming cells migrate to bone resorption site after the resorption. We found that alkaline phosphatase-positive bone forming cells exist around osteoclast-like cell differentiated in soft tissues. Therefore, we hypothesized that osteoclast-derived fluid factor will attract bone forming cells. In our experiment, osteoclast but not macrophage secreted migration factor for mesenchymal stem cells (MSCs) in vitro. Furthermore, MSCs migration was evoked by sphingosine-1-phosphate (S1P) gradient. We are trying to establish knockout cell line of Sphk2, sphingosine kinase 2. Sphk2 KO cell will be an essential tool to investigate precise mechanism by which osteoblast forming cell migrate in bone resorption area.
|
| Academic Significance and Societal Importance of the Research Achievements |
骨粗鬆症は超高齢化社会の日本においては重要な問題である。治療薬として、破骨細胞分化阻害薬は開発されているが、骨形成を促進させる効果を示したものはまだない。そこで、骨吸収から骨形成に転換する因子について研究を行い、破骨細胞が産生分泌するS1Pに骨形成細胞の遊走因子であることが示唆され、今後の骨粗鬆症の治療に役立つと考えられた。
|
