[间歇性压缩力对培养骨细胞转化生长因子β和骨桥蛋白合成的影响]。

M Yamauchi
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引用次数: 0

摘要

长期以来,人们认为骨重塑过程是由骨细胞的连锁反应调控的,涉及化学介质、生长因子和细胞外基质蛋白的合成等。在此背景下,人们也认识到物理刺激是调节骨重塑的重要因素。因此,了解物理刺激是否能够诱导与蛋白质合成的自分泌调节有关的细胞事件至关重要。本研究旨在探讨静水间歇压缩力(ICF)对骨重塑过程中可能起重要作用的转化生长因子β (tgf - β)和基质磷酸化蛋白合成的影响。用含10% FCSP的DMEM培养大鼠骨肉瘤细胞(ROS 17/2.8)。ICF作用于亚融合细胞130 mb, 15/min循环48h。ICF增加了条件培养基的tgf - β活性。这是通过其促进NRK 49F细胞锚定独立生长和抑制人肝癌细胞(Hep-3B)生长的能力来评估的。此外,ICF对Mr. 75 KDa磷酸化蛋白的合成刺激约1.4倍,在5-15%梯度凝胶上通过SDS-PAGE可见。用大鼠骨桥蛋白抗体对磷酸化蛋白进行免疫沉淀,发现75 KDa磷酸化蛋白与骨桥蛋白相同。添加tgf - β抗体可抑制75 KDa骨桥蛋白的合成,并呈剂量依赖性。这些结果表明,ICF刺激了ROS 17/2.8细胞中tgf - β和骨桥蛋白的合成,并且tgf - β可以调节骨桥蛋白的合成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Effects of intermittent compressive force on transforming growth factor beta and osteopontin synthesis in cultured bone cells].

It has long been thought that the process of bone remodeling is regulated by the chain reactions of bone cells involving chemical mediators, growth factors and synthesis of extracellular matrix proteins etc. In this context, it has also been recognized that physical stimulation is an important factor in the regulation of bone remodeling. Thus, it is vitally important to understand whether the physical stimulation can induce the cellular events regarding autocrine regulation of protein synthesis. This study was conducted to examine the effects of hydrostatic intermittent compressive force (ICF) on the synthesis of the transforming growth factor beta (TGF-beta) and matrix phosphoproteins which may play an important role in the process of bone remodeling. The rat osteosarcoma cells (ROS 17/2.8) were cultured with DMEM containing 10% FCSP. ICF was applied to sub-confluent cells at 130 mb, 15/min cycle for 48h. ICF increased TGF-beta activity of the conditioned medium. This was assessed by its capacity to promote anchorage independent growth of NRK 49F cells and to inhibit the growth of human hepatoma cells (Hep-3B). Furthermore, ICF stimulated the synthesis of the phosphoproteins with Mr. 75 KDa by about 1.4 fold which was visualized by SDS-PAGE on 5-15% gradient gel. Immunoprecipitation of the phosphoproteins with rat osteopontin antibody revealed that the 75 KDa phosphoprotein was identical to osteopontin. The 75 KDa osteopontin synthesis was inhibited by the addition of TGF-beta antibody in a dose dependent manner. These results suggested that ICF stimulated the synthesis of TGF-beta and osteopontin in ROS 17/2.8 cells and that the osteopontin synthesis could be regulated by TGF-beta.

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