The role of cell cortex structures in mechanical stress signal transduction in osteoblasts.

张应力（TS）已被证明可以刺激小鼠颅骨缝中的骨生成。为了阐明粘附复合物和细胞骨架在这一机制中的作用，我们研究了这种应激缝细胞的形态学变化。有些用Alexa鬼笔环肽染色，用共聚焦激光扫描显微镜观察它们的肌动蛋白纤维，另一些用TEM观察。结果表明，在缝中的成熟成骨细胞中，肌动蛋白在细胞皮质中积累。在前成骨细胞和成纤维细胞中，观察到肌动蛋白作为应力纤维样结构。成纤维细胞比前成骨细胞厚。在拉伸应力作用3或6小时后，缝线中的所有细胞都在拉伸应力的方向上被拉伸和拉长。肌动蛋白细胞骨架的形态学变化与细胞形态的变化相一致。在拉伸应力6小时的缝合线的细胞中，肌动蛋白应力纤维样结构和肌动蛋白细胞皮质的厚度增加，但在3小时应力组中，它们没有明显增加。细胞粘附分子之一钙粘蛋白在成骨细胞的细胞皮质中沿着分布。另一方面，β-catenin和vinculin的免疫活性在张应力组的成骨细胞中沿沿着细胞皮质增强。

Tensile stress (TS) has been shown to stimulate osteogenesis in the cranial suture of mouse calvaria. In order to clarify the role of the adhesion complex and cytoskeleton in this mechanism, the morphological changes in such stressed suture cells were investigated.TS was applied to the cranial suture of neonatal mouse calvaria in culture. Some were stained with Alexa phalloidin and their actin fibers observed with confocal laser scanning microscopy, with others being observed with TEM. The results show that in the mature osteoblasts in the suture, actin was accumulated in the cell cortex. In the preosteoblastic cells and fibroblastic cells, actin was observed as stress fiber-like structures. Those were thicker in fibroblastic cells than in the preosteoblastic cells. With the tensile stress for 3 or 6 hours, all the cells in the sutures were stretched and elongated in the direction of the tensile stress. Morphological change of actin-cytoskeleton was observed consistent with the change of the cell shape. Thickness of the actin stress fiber-like structure and actin cell cortex were increased in the cells of the tensile stressed suture for 6 hours, but they were not clearly increased in the 3 hour-stressed group. Cadherin, one of the cell adhesion molecules, was observed along the cell cortex of osteoblasts at any experimental time course. On the other hand, immunological activities of β-catenin and vinculin became intense along the cell cortex in the osteoblasts of the tensile stressed groups.