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Towards the understanding of cytoskeleton fluidisation-solidification regulation

机译:为了了解细胞骨架流化 - 凝固调控

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The understanding of the self-regulation of the mechanical properties in non-sarcomeric cells, such as lung cells or cells during tissue development, remains an open research problem with many unresolved issues. Their behaviour is far from the image of the traditionally studied sarcomeric cells, since the crosstalk between the signalling pathways and the complexity of the mechanical properties creates an intriguing mechano-chemical coupling. In these situations, the inelastic effects dominate the cytoskeletal structure showing phenomena like fluidisation and subsequent solidification. Here, we proposes the inelastic contractile unit framework as an attempt to reconciles these effects. The model comprises a mechanical description of the nonlinear elasticity of the cytoskeleton incorporated into a continuum-mechanics framework using the eighth-chains model. In order to address the inelastic effect, we incorporate the dynamic of crosslinks, considering the -actinin and the active stress induced by the myosin molecular motors. Finally, we introduce a hypothesis that links the ability to fluidise and re-solidify as a consequence of the interaction between the active stress and the gelation state defined by the crosslinks. We validate the model with data obtained from experiments of drug-induced relaxation reported in the literature.
机译:理解在组织发育期间肺细胞或细胞如肺细胞等非糖细胞的机械性能的自我调节仍然是许多未解决的问题的开放研究问题。它们的行为远离传统上研究的肉瘤细胞的图像,因为信号传导途径与机械性能的复杂性之间的串扰产生了有趣的机械化学偶联。在这些情况下,非弹性效果主要占据细胞骨架结构,显示出流动化和随后的凝固性的现象。在这里,我们提出了非弹性收缩单元框架作为调和这些效果的尝试。该模型包括使用第八链模型结合到连续式电力框架中的细胞骨架的非线性弹性的力学描述。为了解决不弹性效果,我们掺入交联的动态,考虑到肌苷分子电机诱导的-Actinin和活性应激。最后,我们介绍了一种假设,其将流化的能力链接和重新固化,因为通过交联的主动应力和凝胶态之间的相互作用。我们通过在文献中报告的药物诱导的放松实验中获得的数据验证模型。

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