| Project/Area Number |
14571779
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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 | Nihon University |
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Principal Investigator |
KAWARA Misao Nihon University, School of Dentistry at Matsudo, Professor, 松戸歯学部, 教授 (20147713)
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| Co-Investigator(Kenkyū-buntansha) |
ABIKO Yoshimitsu Nihon University, School of Dentistry at Matsudo, Professor, 松戸歯学部, 教授 (70050086)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | MC3T3-E1 / H_2O_2 / Bone Nodule Formation / gene expression / Free Radical / H_2O_2 / 細胞外基質 / 老化 / 骨芽細胞 / マイクロアレイ / 活性酸素 / マイクロアレイ解析 |
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| Research Abstract |
It is well known that bone formation steadily declines with age resulting in significant loss of bone mass. It is generally believed that the loss of bone in senescence is due to an important of bone formation and an increase of bone resorption. A currently popular hypothesis postulates that the oxygen free radical or reactive oxygen species, of which there are several types, produced during normal cellular metabolism, is a major contributor to the ageing process. Active oxygen species are generally toxic to living cells because they modify and damage various biologically important molecules. It is also well known that free radical such as superoxide anion and nitric oxide have been shown to play a role of osteoclastic bone resorption. We previously reported that bone nodule formation by rat calvarial osteoblasts was reduced when the cells were cultured on hydroxy radical treated fibronectin substratum in vitro. Further, alkaline phosphatase activity and secretion of type 1 collagen as well as those mRNA levels were decreased by hydroxy radical treated FN substratum. These findings suggested that the hydroxy radical damaged FN molecules and reduced the bone formation of osteoblast cells via inhibition of proliferation and/or differentiation of osteoblast progenitors and the calcification process.
The purpose of this study is to establish the cell culture system to investigate the effect of H_2O_2 on osteoblast function involved in bone mineralization rate using MC3T3-E1 cells. Taken together with previous study and our present study, it is conceivable that oxidative stress is important role of bone resorption and bone formation. Therefore, experimental models such as presented here may also be useful investigating osteoblast function an ageing. In conclusion, the oxidative stress produced during ageing affect bone-related gene expression and cell differentiation, and it cause the reduction of mineralization of osteoblasts.
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