Much is known about the biophysical mechanisms involved in cell crawling, but how these processes are coordinated to produce directed motion is not well understood. Here, we propose a new hypothesis whereby local cytoskeletal contraction generates fluid flow through the lamellipodium, with the pressure at the front of the cell facilitating actin polymerization which pushes the leading edge forward. The contraction, in turn, is regulated by stress in the cytoskeleton. To test this hypothesis, finite element models for a crawling cell are presented. These models are based on nonlinear poroelasticity theory, modified to include the effects of active contraction and growth, which are regulated by mechanical feedback laws. Results from the models agree reasonably well with published experimental data for cell speed, actin flow, and cytoskeletal deformation in migrating fish epidermal keratocytes. The models also suggest that oscillations can occur for certain ranges of parameter values.

中文翻译：

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细胞爬行的多孔弹性模型，包括细胞骨架收缩和肌动蛋白聚合之间的机械耦合

关于细胞爬行所涉及的生物物理机制有很多了解，但这些过程如何协调以产生定向运动尚不清楚。在这里，我们提出了一个新的假设，即局部细胞骨架收缩产生流体流过 lamellipodium，细胞前部的压力促进肌动蛋白聚合，推动前缘向前。反过来，收缩受细胞骨架中的压力调节。为了检验这一假设，我们提出了爬行细胞的有限元模型。这些模型基于非线性多孔弹性理论，经过修改以包括受机械反馈定律调节的主动收缩和生长的影响。模型结果与已发表的细胞速度、肌动蛋白流量、和迁移鱼表皮角质细胞的细胞骨架变形。这些模型还表明，某些参数值范围可能会发生振荡。