Mechanotransduction and strain amplification in osteocyte cell processes
Mechanotransduction and strain amplification in osteocyte cell processes
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DOI：
10.1073/pnas.0407429101
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发表时间：
2004-11-23
影响因子：
11.1
通讯作者：
Weinbaum, S
中科院分区：
文献类型：
--
作者：
Han, YF;Cowin, SC;Weinbaum, S
骨组织中的一个矛盾是，由于动物和人类运动引起的组织水平的应变太小，无法直接启动细胞内的化学反应。最近提出了一个模型来解决这个矛盾，它预测，由于机械负荷，通过细胞周围基质中的腔隙-小管孔隙度的流体流动可以诱导应变的肌动蛋白丝束的细胞骨架是一个以上的数量级大于组织水平的应变。在这项研究中，我们极大地完善了这个模型，通过使用最新的超微结构数据的细胞过程细胞骨架，拴系元素，附加的过程中的小管壁和他们的有限的抗弯刚度EL。我们构建了一个更现实的3D模型的骨细胞的过程，然后使用大变形的“弹性”理论有限EL预测的拴系元素和中央肌动蛋白束上的环向应变的变形形状。我们的模型预测的细胞过程比先前的研究中的刚性高3倍，但是对于在1 Hz下> 1，000微应变的组织水平应变和在> 10 Hz下> 250微应变的组织水平应变，环向应变> 0.5%。我们建议，这种应变放大模型提供了一个更可能的假设比以前提出的流体剪切假说的骨细胞的兴奋。
A paradox in bone tissue is that tissue-level strains due to animal and human locomotion are too small to initiate intracellular chemical responses directly. A model recently was proposed to resolve this paradox, which predicts that the fluid flow through the pericellular matrix in the lacunar-canalicular porosity due to mechanical loading can induce strains in the actin filament bundles of the cytoskeleton that are more than an order of magnitude larger than tissue level strains. In this study, we greatly refine this model by using the latest ultrastructural data for the cell process cytoskeleton, the tethering elements that attach the process to the canalicular wall and their finite flexural rigidity El. We construct a much more realistic 3D model for the osteocyte process and then use large-deformation "elastica" theory for finite El to predict the deformed shape of the tethering elements and the hoop strain on the central actin bundle. Our model predicts a cell process that is 3 times stiffer than in a previous study but hoop strain of > 0.5% for tissue-level strains of > 1,000 microstrain at 1 Hz and > 250 microstrain at frequencies > 10 Hz. We propose that this strain-amplification model provides a more likely hypothesis for the excitation of osteocytes than the previously proposed fluid-shear hypothesis.