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首页> 外文期刊>American Journal of Physiology >Rat airway smooth muscle cell during actin modulation: rheology and glassy dynamics.
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Rat airway smooth muscle cell during actin modulation: rheology and glassy dynamics.

机译：肌动蛋白调节过程中的大鼠气道平滑肌细胞：流变学和玻璃态动力学。

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Although changes of cytoskeleton (CSK) stiffness and friction can be induced by diverse interventions, all mechanical changes reported to date can be scaled onto master relationships that appear to be universal. To assess the limits of the applicability of those master relationships, we focused in the present study on actin and used a panel of actin-manipulating drugs that is much wider than any used previously. We focused on the cultured rat airway smooth muscle (ASM) cell as a model system. Cells were treated with agents that directly modulate the polymerization (jasplakinolide, cytochalasin D, and latrunculin A), branching (genistein), and cross linking (phallacidin and phalloidin oleate) of the actin lattice. Contractile (serotonin, 5-HT) and relaxing (dibutyryl adenosine 3',5'-cyclic monophosphate, DBcAMP) agonists and a myosin inhibitor (ML-7) were also tested for comparison, because these agents may change the structure of actin indirectly. Using optical magnetic twisting cytometry, we measured elastic and frictional moduli before and after treatment with each agent. Stiffness increased with frequency as a weak power law, and changes of friction paralleled those of stiffness until they approached a Newtonian viscous limit. Despite large differences in the mechanism of action among the interventions, all data collapsed onto master curves that depended on a single parameter. In the context of soft glassy systems, that parameter would correspond to an effective temperature of the cytoskeletal matrix and reflect the effects of molecular crowding and associated molecular trapping. These master relationships demonstrate that when the mechanical properties of the cell change, they are constrained to do so along a special trajectory. Because mechanical characteristics of the cell shadow underlying molecular events, these results imply special constraints on the protein-protein interactions that dominate CSK mechanical properties.
机译：尽管可以通过多种干预措施来诱导细胞骨架（CSK）刚度和摩擦力的变化，但迄今为止报道的所有机械变化都可以按比例显示在似乎普遍的主要关系上。为了评估这些主要关系的适用范围，我们在本研究中重点研究了肌动蛋白，并使用了一系列肌动蛋白操纵药物，其作用范围比以前使用的任何药物都宽得多。我们将培养的大鼠气道平滑肌（ASM）细胞作为模型系统。用直接调节肌动蛋白晶格的聚合反应（茉莉香菊酯，细胞松弛素D和latrunculin A），分支（染料木黄酮）和交联（phallacidin和鬼笔环素油酸酯）的试剂处理细胞。还测试了收缩性（5-羟色胺，5-HT）和松弛性（二丁酰腺苷3'，5'-环一磷酸，DBcAMP）激动剂和肌球蛋白抑制剂（ML-7）进行比较，因为这些试剂可能间接改变肌动蛋白的结构。 。使用光学磁扭细胞术，我们测量了每种药物治疗前后的弹性模量和摩擦模量。作为弱幂律，刚度随频率增加，而摩擦的变化与刚度的变化平行，直到达到牛顿粘性极限。尽管干预之间的作用机制差异很大，但所有数据都折叠到依赖于单个参数的主曲线上。在软玻璃系统的背景下，该参数将对应于细胞骨架基质的有效温度，并反映分子拥挤和相关分子捕获的影响。这些主要关系表明，当细胞的机械性能发生变化时，它们会被约束沿着特定的轨迹进行变化。由于分子事件背后的细胞阴影的机械特性，这些结果暗示着对主导CSK机械性能的蛋白质-蛋白质相互作用的特殊限制。

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