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机械力诱导 TGFB1 增加 hPDL 细胞中 SOST/POSTN 的表达。

Mechanical Force-induced TGFB1 Increases Expression of SOST/POSTN by hPDL Cells.

机构信息

Department of Anatomy, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand Mineralized Tissue Research Unit, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.

Graduate School, Faculty of Engineering, Thai-Nichi Institute of Technology, Bangkok, Thailand.

出版信息

J Dent Res. 2015 Jul;94(7):983-9. doi: 10.1177/0022034515581372. Epub 2015 Apr 13.

Abstract

The aim of this study was to investigate the response of human periodontal ligament (hPDL) fibroblasts to an intermittent compressive force and its effect on the expression of SOST, POSTN, and TGFB1. A computerized cell compressive force loading apparatus was introduced, and hPDL cells were subjected to intermittent compressive force. The changes in messenger RNA (mRNA) and protein expression were monitored by real-time polymerase chain reaction and Western blot analysis, respectively. An increased expression of SOST, POSTN, and TGFB1 was observed in a time-dependent fashion. Addition of cycloheximide, a transforming growth factor (TGF)-β inhibitor (SB431542), or a neutralizing antibody against TGF-β1 attenuated the force-induced expression of SOST and POSTN as well as sclerostin and periostin, indicating a role of TGF-β1 in the pressure-induced expression of these proteins. Enzyme-linked immunosorbent assay analysis revealed an increased level of TGF-β1 in the cell extracts but not in the medium, suggesting that intermittent compressive force promoted the accumulation of TGF-β1 in the cells or their surrounding matrix. In conclusion, an intermittent compressive force regulates SOST/POSTN expression by hPDL cells via the TGF-β1 signaling pathway. Since these proteins play important roles in the homeostasis of the periodontal tissue, our results indicate the importance of masticatory forces in this process.

摘要

本研究旨在探讨人牙周韧带(hPDL)成纤维细胞对间歇压力的反应及其对 SOST、POSTN 和 TGFB1 表达的影响。引入了计算机化细胞压缩力加载装置,并对 hPDL 细胞施加间歇压力。通过实时聚合酶链反应和 Western blot 分析分别监测信使 RNA(mRNA)和蛋白质表达的变化。SOST、POSTN 和 TGFB1 的表达呈时间依赖性增加。加入环加氧酶抑制剂(SB431542)或 TGF-β1 的中和抗体可减弱力诱导的 SOST 和 POSTN 以及骨硬化蛋白和骨粘连蛋白的表达,表明 TGF-β1 在这些蛋白的压力诱导表达中起作用。酶联免疫吸附分析显示细胞提取物中 TGF-β1 水平增加,但培养基中没有增加,表明间歇压力促进了 TGF-β1 在细胞内或周围基质中的积累。总之,间歇压力通过 TGF-β1 信号通路调节 hPDL 细胞中 SOST/POSTN 的表达。由于这些蛋白在牙周组织的动态平衡中发挥重要作用,我们的结果表明咀嚼力在这一过程中的重要性。

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