Involvement of PPAR γ in senescence-induced osteoporosis
| Project/Area Number |
12671799
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
MORITA Ikuo Tokyo Medical and Dental University, Graduate School, Associate Professor, 大学院・医歯学総合研究科, 助教授 (60100129)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Osteoblasts / Adipocytes / Osteoclasts / PPAR / Cbfa-1 / CBP / α / Human mesenchymal cells / 骨芽細胞分化 / 脂肪細胞分化 / BMP-2 / PPARγ / 老人性骨粗鬆症 / 間葉系幹細胞 |
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| Research Abstract |
Senescence-induced osteoporosis is thought to be a low turnover type and to be due to the shift from osteoblastogenesis to adipogenesis. In this study, we investigated the effects of some drugs affected bone metabolism on adipose differentiation and the effects of adipogenesis on osteoclastogenesis and osteoblastogenesis. We used mouse preosteoblast cell lines established in our laboratory and human mesenchymal stem cells isolated from bone marrow. The PPARγ ligands such as 15-deoxy.-Δ 12,14-PGJ2 and trogritazone stimulated adipogenesis, but IL-11 and vitaminK2 suppressed the adipogenesis. The adipocyte differentiation caused to decrease the osteoclast formation-supporting activity, but did not affect osteoblastogenesis. The similar results were obtained from in vivo study. When human mesenchymal cells with BMP-2 and vitamin K2 inoculated to Matrigel and transplanted subcutaneously to nude mice, the cells was differentiated to osteoblasts and adipocytes by BMP-2. The effect of vitamin K2 on osteoblastogenesis failed to be observed in spite of the suppression of adipogenesis.
These data indicate that the suppression of adipogenesis is not benefit for the protect of senescence-induced osteoporosis.
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Report
(3 results)
Research Products
(9 results)
