The development of implant surface to promote soft tissue integration using real-time cell analysis

本研究的目的是检测机械应力诱导的小鼠牙龈上皮细胞炎症介质。为了确定静态压缩力的作用，将GE 1细胞在三维胶原凝胶系统（3D-凝胶）中培养。使用放置在凝胶上的钛板施加压缩力，通过增加重量来调节。GE_1细胞在2.5~10.0g/cm ~ 2压力作用下3 h，或在7.5g/cm ~ 2压力作用下1~ 48 h。在施加压力后，提取总RNA，并通过RT-PCR分析考克斯-1和考克斯-2的表达水平。通过ELISA测量释放到培养基中的PGE 2的量。在7.5g/cm ^2的压力下，GE 1细胞中考克斯-2 mRNA的表达呈力依赖性增加。时程实验显示，细胞培养6 h后，考克斯-2 mRNA表达增加，12 h后表达略有下降。另一方面，考克斯-1 mRNA的表达没有改变。与对照组相比，压力促进了条件培养基中PGE 2的释放。这些结果表明，机械应力增强了GE 1细胞的PGE 2产量。

The purpose of this study is to examine the inflammatory mediators induced by mechanical stress in mouse gingival epithelial cells. In order to determine the effect of static compressive force, GE1 cells were cultured in a three dimensional collagen gel system (3D-gel). Compressive force was applied using titanium plate placed over the gels, which was adjusted by adding weight. GE1 cells were subjected to 2.5~10.0g/cm^2 of compressive force for 3h, or 7.5g/cm^2 for 1~48h. After the application of compressive force, total RNA was extracted and the expression levels of COX-1 and COX-2 were analyzed by RT-PCR. The amount of PGE2 released into culture medium was measured by ELISA. Under the compressive force, the expression of COX-2 mRNA in GE1 cells increased in a force dependent manner up to 7.5g/cm^2. The time-course experiment showed that COX-2 mRNA increased when the cells were cultured for 6h, but the expression slightly reduced after 12h. On the other hand, COX-1 mRNA expression was not changed. The compressive force enhances the release of PGE2 in the conditioned medium compared with the control group. These results demonstrated that mechanical stress enhanced PGE2 production from GE1 cells.