Gunst Susan J, Tang Dale D, Opazo Saez Anabelle
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN 46202-5120, USA.
Respir Physiol Neurobiol. 2003 Sep 16;137(2-3):151-68. doi: 10.1016/s1569-9048(03)00144-7.
Airway smooth muscle is continuously subjected to mechanical forces caused by changes in lung volume during breathing. These mechanical oscillations have profound effects on airway smooth muscle contractility both in vivo and in vitro. Alterations in airway smooth muscle properties in response to mechanical forces may result from adaptive changes in the organization of the actin cytoskeleton. Recent advances suggest that in airway smooth muscle, two cytosolic signaling proteins that associate with focal adhesion complexes, focal adhesion kinase (FAK) and paxillin, are involved in transducing external mechanical signals. FAK and paxillin regulate changes in the organization of the actin cytoskeleton and the activation of contractile proteins. Actin is in a dynamic state in airway smooth muscle and undergoes polymerization and depolymerization during the contraction-relaxation cycle. The organization of the cytoskeletal proteins, vinculin, talin, and alpha-actinin, which mediate linkages between actin filaments and transmembrane integrins, is also regulated by contractile stimulation in airway smooth muscle. The fluidity of the cytoskeletal structure of the airway smooth muscle cell may be fundamental to its ability to adapt and respond to the mechanical forces imposed on it in the lung during breathing.
气道平滑肌在呼吸过程中持续受到肺容积变化所产生的机械力作用。这些机械振荡对体内和体外的气道平滑肌收缩性均有深远影响。气道平滑肌特性因机械力而发生的改变可能源于肌动蛋白细胞骨架组织的适应性变化。最近的研究进展表明，在气道平滑肌中，两种与粘着斑复合体相关的胞质信号蛋白，即粘着斑激酶（FAK）和桩蛋白，参与了外部机械信号的转导。FAK和桩蛋白调节肌动蛋白细胞骨架组织的变化以及收缩蛋白的激活。肌动蛋白在气道平滑肌中处于动态状态，在收缩-舒张周期中经历聚合和解聚。介导肌动蛋白丝与跨膜整合素之间连接的细胞骨架蛋白、纽蛋白、踝蛋白和α-辅肌动蛋白的组织也受到气道平滑肌收缩刺激的调节。气道平滑肌细胞细胞骨架结构的流动性可能是其在呼吸过程中适应并响应肺部施加于其上的机械力的能力的基础。
