Smith P G, Tokui T, Ikebe M
Department of Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Am J Physiol. 1995 Jun;268(6 Pt 1):L999-1005. doi: 10.1152/ajplung.1995.268.6.L999.
Smooth muscle hypertrophy is often found in tissue subjected to abnormal physical stress. To determine if physical stress (strain) per se could increase the contractile potential of airway smooth muscle (ASM), we compared cultured ASM cells subjected to strain to control cells (no strain) for rates of 1) myosin light chain kinase (MLCK)-mediated myosin light chain (LC20) phosphorylation, 2) actin-activated myosin ATPase, and 3) myosin light chain phosphatase-mediated myosin dephosphorylation. Lysates from strained cells showed increases in both LC20 phosphorylation activity and actomyosin ATPase activity but decreased rates of phosphatase-dependent myosin dephosphorylation. The increased LC20 phosphorylation activity and ATPase activity of the strained cells were accompanied by increases in cellular content of MLCK and myosin, respectively, compared with control. Because the cultured ASM cells exposed to strain expressed higher MLCK activity and actomyosin ATPase activity but lower myosin light chain phosphatase activity, these data suggest that physical stress in part determines ASM potential for contractile state.
平滑肌肥大常见于遭受异常物理应激的组织中。为了确定物理应激(应变)本身是否会增加气道平滑肌(ASM)的收缩潜能,我们将经受应变的培养ASM细胞与对照细胞(无应变)在以下方面进行了比较:1)肌球蛋白轻链激酶(MLCK)介导的肌球蛋白轻链(LC20)磷酸化速率、2)肌动蛋白激活的肌球蛋白ATP酶以及3)肌球蛋白轻链磷酸酶介导的肌球蛋白去磷酸化速率。经受应变的细胞裂解物显示LC20磷酸化活性和肌动球蛋白ATP酶活性均增加,但磷酸酶依赖性肌球蛋白去磷酸化速率降低。与对照相比,经受应变的细胞中增加的LC20磷酸化活性和ATP酶活性分别伴随着MLCK和肌球蛋白细胞含量的增加。由于暴露于应变的培养ASM细胞表现出较高的MLCK活性和肌动球蛋白ATP酶活性,但肌球蛋白轻链磷酸酶活性较低,这些数据表明物理应激在一定程度上决定了ASM的收缩状态潜能。