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Sarcomeric model of stretch-induced stress fiber reorganization

机译：拉伸诱导应力纤维重组的肌节模型

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Abstract: Actin stress fibers (SFs) are mechanosensitive structural elements that respond to applied stress and strain to regulate cell morphology, signal transduction, and cell function. Results from various studies indicate that SFs tend to maintain stress or strain at a constant level. We developed a simple quantitative sarcomeric model of SFs to predict the role of actomyosin crossbridge cycling in SF tension regulation and reorientation in response to cyclic stretching. Under static conditions, the steady-state levels of SF tension were determined by the fiber passive stiffness and the stall force of the constituent myosin II filaments. When subject to cyclic changes in length at low frequencies, SFs change their unloaded reference length levels through myosin sliding to maintain tension at the original level. At high stretch frequencies, myosin cannot respond quickly enough and the SF behaves elastically. Myosin sliding also contributes to SF turnover, resulting in SF reorientation away from the direction of stretching at high, but not low, stretch frequencies. Using model parameters extracted from the literature, our model describes the dependence of cyclic stretch-induced SF alignment on stretch frequency and pattern consistent with experimental findings. This analysis predicts that myosin II plays multiple roles in regulating the ability of SFs to adapt to a dynamic mechanical environment.
机译：摘要：肌动蛋白应力纤维（SFs）是机械敏感的结构元件，可对施加的应力和应变作出响应，以调节细胞的形态，信号转导和细胞功能。各种研究的结果表明，SF倾向于将压力或应变保持在恒定水平。我们开发了一个简单的SF定量肌节模型，以预测肌动球蛋白跨桥循环在SF张力调节和响应循环拉伸中的重新定向中的作用。在静态条件下，SF张力的稳态水平取决于纤维的被动刚度和组成肌球蛋白II丝的失速力。当低频下长度周期性变化时，SF通过肌球蛋白滑动改变其空载参考长度水平，以将张力保持在原始水平。在高拉伸频率下，肌球蛋白不能足够迅速地反应并且SF表现出弹性。肌球蛋白的滑动也有助于SF的周转，导致SF在高但不低的拉伸频率下偏离拉伸方向重新定向。使用从文献中提取的模型参数，我们的模型描述了循环拉伸诱导的SF对准对拉伸频率和模式的依赖性，与实验结果一致。这项分析预测，肌球蛋白II在调节SF适应动态机械环境的能力中起多种作用。

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