中文摘要：

骨头质量上的前列腺素 E2 (PGE2 ) 的效果在 vivo 是生长得很好的。以前的研究证明了 PGE2 增加区别，增长，并且在静态地有教养的造骨细胞通过 F 肌动朊压力纤维调整房间形态学。然而，造骨细胞上的 PGE2 的效果面对液体砍应力(FSS ) 它能更好揭开在 vivo 的 PGE2 的 anabolism 的效果，还得被检验。这里，我们假设了那 PGE2 通过蛋白质 kinase A (PKA ) 在刺激 FSS 的 MC3T3-E1 osteoblastic 房间调制 F 肌动朊压力纤维小径。而且，改变的这导致 PGE2 的 F 肌动朊与细胞的 mechanosensitivity 的恢复被联系。我们的数据证明有为 15 min 的 10 nM dmPGE2 的处理显著地以一种 PKA 依赖的方式在刺激 FSS 的房间压制了 F 肌动朊压力纤维紧张。另外， dmPGE2 处理提高了房间的钙山峰大小和在第二 FSS 刺激回答房间的百分比，尽管这些效果被合作处理与 phalloidin 废除并且稀释。我们的结果证明 10 nM dmPGE2 能通过 PKA 小径部分加速 F 肌动朊压力纤维的重设过程到它的预先刺激的水平，并且因此支持了细胞的 mechanosensitivity 的恢复。我们发现 PGE2 由增加了出现在 vivo 的骨头形成的新奇细胞的机制提供，建议那 PGE2 能是为骨头的处理的一个潜在的目标形成相关的疾病。

英文摘要：

The effect of prostaglandin E2（PGE2） on bone mass has been well-established in vivo. Previous studies have showed that PGE2 increases differentiation, proliferation, and regu- lates cell morphology through F-actin stress fiber in statically cultured osteoblasts. However, the effect of PGE2 on osteo- blasts in the presence of fluid shear stress （FSS）, which could better uncover the anabolic effect of PGEz in vivo, has yet to be examined. Here, we hypothesized that PGE2 modulates F-actin stress fiber in FSS-stimulated MC3T3-E1 osteoblastic cells through protein kinase A （PKA） pathway. Furthermore, this PGE2-induced F-actin remodeling was associated with the recovery of cellular mechanosensitivity. Our data showed that treatment with 10 nM dmPGE2 for 15 rain significantly suppressed the F-actin stress fiber intensity in FSS-stimulated cells in a PKA-dependent manner. In addition, dmPGE2 treatment enhanced the cells＇ calcium peak magnitude and the percentage of responding cells in the second FSS stimulation, though these effects were abolished and attenuated by co-treatment with phalloidin. Our results demonstrated that 10 nM dmPGE2 was able to accelerate the ＇reset＇ process of F-actin stress fiber to its pre-stimulated level partially through PKA pathway, and thus promoted the recovery of cellular mechanosensitivity. Our finding provided a novel cellular mechanism by which PGE2 increased bone forma- tion as shown in vivo, suggesting that PGE2 could be a potential target for treatments of bone formation-related diseases.