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Cyclic stretch reveals a mechanical role for intermediate filaments in a desminopathic cell model

机译:循环拉伸揭示了脱丝细胞模型中中间丝的机械作用

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Mechanics is now recognized as crucial in cell function. To date, the mechanical properties of cells have been inferred from experiments which investigate the roles of actin and microtubules ignoring the intermediate filaments (IFs) contribution. Here, we analyse myoblasts behaviour in the context of myofibrillar myopathy resulting from p.D399Y desmin mutation which disorganizes the desmin IF network in muscle cells. We compare the response of myoblasts expressing either mutated or wild-type desmin to cyclic stretch. Cells are cultivated on supports submitted to periodic uniaxial stretch of 20% elongation amplitude and 0.3 Hz frequency. We show that during stretching cycles, cells expressing mutated desmin reduce their mean amplitude both for the elongation and spreading area compared to those expressing wild-type desmin. Even more unexpected, the reorientation angles are altered in the presence of p.D399Y desmin. Yet, at rest, the whole set of those parameters are similar for the two cell populations. Thus, we demonstrate that IFs affect the mechanical properties and the dynamics of cell reorientation. Since these processes are known due to actin cytoskeleton, these results suggest the IFs implication in mechanics signal transduction. Further studies may lead to better understanding of their contribution to this process.
机译:如今,力学被认为对细胞功能至关重要。迄今为止,已经从实验推论了细胞的机械性能,该实验研究了肌动蛋白和微管的作用而忽略了中间丝(IF)的贡献。在这里,我们分析了由p.D399Y desmin突变引起的肌原纤维肌病的成肌细胞行为,该突变使肌肉细胞中的desmin IF网络混乱。我们比较表达突变或野生型结蛋白成环的成肌细胞的反应。在支撑物上培养细胞,使其周期性地进行单轴拉伸,延伸幅度为20%,频率为0.3 Hz。我们表明,在拉伸周期中,与表达野生型结蛋白的细胞相比,表达突变的结蛋白的细胞在延伸和扩散区域均降低了其平均振幅。更令人意外的是,在存在p.D399Y desmin的情况下改变了重新定向角度。然而,静止时,两个细胞群的这些参数的整个集合是相似的。因此,我们证明中频影响机械性能和细胞重新定向的动力学。由于这些过程由于肌动蛋白的细胞骨架而为人所知,因此这些结果表明IFs参与了机械信号转导。进一步的研究可能会导致人们更好地了解他们对该过程的贡献。

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