The function of periostin during periodontal tissue remodeling caused by mechanical stress.
骨膜素在机械应力引起的牙周组织重塑过程中的功能。
基本信息
- 批准号:13470452
- 负责人:
- 金额:$ 10.37万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 财政年份:2001
- 资助国家:日本
- 起止时间:2001 至 2002
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
The periodontal ligament (PDL) plays an important role in the remodeling of the periodontal tissues during orthodontic tooth movement. Many factors are involved in the mechanisms of response to an orthodontic force. One of these factors might be periostin, which has a specific expression in the PDL and the periosteum. Therefore, the aim of this study was to elucidate the role of periostin in the PDL during tooth movement and its effect on osteoclasts. In this study, periostin mRNA expression was investigated using experimental tooth movement model in rats in vivo and the effect of uni-axial mechanical stress was examined on human periodontal ligament fibroblastic cells (hPDLF) in vitro. Also the effect of periostin on osteoclasts was analyzed. In situhybridization assay revealed that periostin mRNA was expressed in the PDL in controls stained with antisense probes. This expression appeared to be stronger in the compression sites compared with the tension sites after 3 hours of starting tooth movement. At 24 hours periostin mRNA showed the highest levels and returned to levels similar to controls after 168 hours. In vitro experiments showed that periostin mRNA expression detected by RT-PCR increased after uni-axial mechanical stress was applied for 24 hours in hPDLF cultures. We also found that periostin had an inhibitory effect on osteoclast differentiation and activation when conditioned medium from mechanically stressed hPDLF was added to human osteoclast culture system. These data was confirmed when similar results were observed in mouse unfractionated bone cell cultures treated with mouse recombinant periostin to a final concentration of 600 ng/ml. In this study, we demonstrated that periostin mRNA expression increased in the PDL during experimental tooth movement in vivo, especially in the compression sites, and was induced by uni-axial mechanical stress in vitro. Furthermore, periostin may inhibit osteoclast differentiation and activation.
牙周膜在正畸牙移动过程中对牙周组织的改建起着重要作用。许多因素参与了正畸力的反应机制。骨膜蛋白可能是其中之一,它在牙周膜和骨膜中有特异性表达。因此,本研究的目的是阐明骨膜蛋白在牙齿移动过程中的PDL中的作用及其对破骨细胞的影响。在这项研究中,periostin mRNA的表达进行了研究,采用实验性牙齿移动模型在大鼠体内和单轴机械应力的影响,在体外人牙周膜成纤维细胞(hPDLF)。分析骨膜蛋白对破骨细胞的影响。原位杂交结果显示,对照组牙周膜中有骨膜蛋白mRNA表达。在开始牙齿移动3小时后,与张力位点相比,这种表达在压缩位点中似乎更强。在24小时,骨膜蛋白mRNA显示出最高水平,并在168小时后恢复到与对照相似的水平。体外实验表明,在hPDLF培养物中施加单轴机械应力24小时后,RT-PCR检测到periostin mRNA表达增加。我们还发现,骨膜蛋白对破骨细胞的分化和激活有抑制作用时,从机械应力hPDLF条件培养基中加入人破骨细胞培养系统。当在用小鼠重组骨膜蛋白处理至终浓度为600 ng/ml的小鼠未分级骨细胞培养物中观察到类似结果时,证实了这些数据。在这项研究中,我们证明,periostin mRNA的表达增加,在实验性牙齿移动在体内的PDL,特别是在压缩的网站,并在体外诱导的单轴机械应力。此外,骨膜蛋白可抑制破骨细胞的分化和活化。
项目成果
期刊论文数量(40)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Nishi M: "A missense mutant myostatin causes hyperplasia without hypertrophy in the mouse muscle"Biochem Biophys Res Commun. 293・1. 241-251 (2002)
Nishi M:“错义突变体肌生长抑制素导致小鼠肌肉增生而不肥大”Biochem Biophys Res Commun.293·1(2002)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Hatai T.: "Apoptosis of periodontal ligament cells induced by mechanical stress during tooth movement"Oral Dis.. 7. 287-290 (2001)
Hatai T.:“牙齿移动过程中机械应力诱导的牙周膜细胞凋亡”Oral Dis.. 7. 287-290 (2001)
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Abe M: "Role for macrophage inflammatory protein (MIP)-1alpha and MIP-1beta in the development of osteolytic lesions in multiple myeloma"Blood. 100・6. 2195-2202 (2002)
Abe M:“巨噬细胞炎症蛋白(MIP)-1α和MIP-1β在多发性骨髓瘤溶骨性病变发展中的作用”血液100・6(2002)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
泰江章博: "骨格筋形成におけるマイオスタチンの役割"生命の科学. 52(4). 256-260 (2001)
Akihiro Yasue:“肌肉生长抑制素在骨骼肌形成中的作用”《生命科学》52(4)。
- DOI:
- 发表时间:
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- 影响因子:0
- 作者:
- 通讯作者:
Ueno A, Kitase Y, Moriyama K, Inoue H: "MC3T3-E1-conditioned medium-induced mineralization by clonal rat dental pulp cells."Matrix Biol.. 20(5-6). 347-355 (2001)
Ueno A、Kitase Y、Moriyama K、Inoue H:“MC3T3-E1 条件培养基诱导克隆大鼠牙髓细胞矿化。”Matrix Biol.. 20(5-6)。
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- 影响因子:0
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MORIYAMA Keiji其他文献
MORIYAMA Keiji的其他文献
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23659963 - 财政年份:2011
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18209060 - 财政年份:2006
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