Mechanical strain increases velocity and extent of shortening in cultured airway smooth muscle cells.

Mechanical strain increases velocity and extent of shortening in cultured airway smooth muscle cells.
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机械应变增加了培养的气道平滑肌细胞的缩短速度和程度。

DOI:
10.1152/ajplung.1999.277.2.l343
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发表时间:
1999
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Brozovich,F
Brozovich,F
中科院分区:
--
文献类型:
--
作者:
Smith,PG;Roy,C;Dreger,J;Brozovich,F

文献摘要

被引文献

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肺组织上的异常机械应力与气道平滑肌(ASM)的质量和收缩性增加有关。我们已经报道,培养的ASM细胞进行周期性应变表现出增加肌球蛋白轻链激酶(MLCK)和应力丝。增加MLCK可能会增加收缩速度,而增加应力丝可以通过增加细胞的内部负荷来阻止细胞缩短。为了研究应变诱导的细胞收缩性变化,记录暴露于90 mM KCl的单个细胞缩短的时间过程。长度与时间图显示应变细胞的最大缩短速度显著大于对照组(无应变)。这与单独实验中在品系细胞中测量的MLCK和肌球蛋白轻链磷酸化增加相关。应变细胞中细胞缩短的程度往往更大,因此未检测到对缩短的阻抗增加。因此,机械应力可能通过增加MLCK的含量来增加ASM的收缩性。
Abnormal mechanical stress on lung tissue is associated with increased mass and contractility of airway smooth muscle (ASM). We have reported that cultured ASM cells subjected to cyclic strain exhibit increased myosin light chain kinase (MLCK) and stress filaments. Increased MLCK may increase contractile velocity, whereas increased stress filaments could impede cell shortening by increasing the cell’s internal load. To study strain-induced changes in cell contractility, the time course of shortening of individual cells exposed to 90 mM KCl was recorded. Length vs. time plots revealed significantly greater maximal velocity of shortening in strain cells than control (no strain). This correlated with an increase in MLCK and myosin light chain phosphorylation measured in strain cells in separate experiments. The extent of cell shortening tended to be greater in the strain cells so that increased impedance to shortening was not detected. Mechanical stress may therefore increase the contractility of ASM by increasing the content of MLCK.