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首页> 外文期刊>American Journal of Physiology >Stiffness changes in cultured airway smooth muscle cells.
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Stiffness changes in cultured airway smooth muscle cells.

机译：培养的气道平滑肌细胞的硬度变化。

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Airway smooth muscle (ASM) cells in culture stiffen when exposed to contractile agonists. Such cell stiffening may reflect activation of the contractile apparatus as well as polymerization of cytoskeletal biopolymers. Here we have assessed the relative contribution of these mechanisms in cultured ASM cells stimulated with serotonin (5-hydroxytryptamine; 5-HT) in the presence or absence of drugs that inhibit either myosin-based contraction or polymerization of filamentous (F) actin. Magnetic twisting cytometry was used to measure cell stiffness, and associated changes in structural organization of actin cytoskeleton were evaluated by confocal microscopy. We found that 5-HT increased cell stiffness in a dose-dependent fashion and also elicited rapid formation of F-actin as marked by increased intensity of FITC-phalloidin staining in these cells. A calmodulin antagonist (W-7), a myosin light chain kinase inhibitor (ML-7) and a myosin ATPase inhibitor (BDM) each ablated the stiffening response but not the F-actin polymerization induced by 5-HT. Agents that inhibited the formation of F-actin (cytochalasin D, latrunculin A, C3 exoenzyme, and Y-27632) attenuated both baseline stiffness and the extent of cell stiffening in response to 5-HT. Together, these data suggest that agonist-evoked stiffening of cultured ASM cells requires actin polymerization as well as myosin activation and that neither actin polymerization nor myosin activation by itself is sufficient to account for the cell stiffening response.
机译：当暴露于收缩性激动剂时，培养物中的气道平滑肌（ASM）细胞变硬。这种细胞变硬可以反映收缩装置的活化以及细胞骨架生物聚合物的聚合。在这里，我们评估了在存在或不存在抑制基于肌球蛋白的收缩或丝状肌动蛋白聚合反应的药物的情况下，用5-羟色胺（5-羟色胺; 5-HT）刺激的培养的ASM细胞中这些机制的相对贡献。磁扭细胞术用于测量细胞硬度，并通过共聚焦显微镜评估肌动蛋白细胞骨架结构组织的相关变化。我们发现5-HT以剂量依赖的方式增加了细胞的硬度，并且还引起了F-肌动蛋白的快速形成，其特征是这些细胞中FITC-鬼笔环肽染色的强度增加。钙调蛋白拮抗剂（W-7），肌球蛋白轻链激酶抑制剂（ML-7）和肌球蛋白ATPase抑制剂（BDM）均能消除增强反应，但不能消除5-HT诱导的F-肌动蛋白聚合。抑制F-肌动蛋白（细胞松弛素D，latrunculin A，C3外切酶和Y-27632）形成的药物会减弱基线硬度和对5-HT的反应细胞僵硬程度。总之，这些数据表明培养的ASM细胞的激动剂引起的硬化需要肌动蛋白聚合以及肌球蛋白活化，并且肌动蛋白聚合或肌球蛋白活化本身都不足以说明细胞的硬化反应。

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