The Smooth Muscle Research Group, Department of Physiology & Pharmacology, Faculty of Medicine, University of Calgary, Canada.
Arch Biochem Biophys. 2011 Jun 15;510(2):160-73. doi: 10.1016/j.abb.2011.02.024. Epub 2011 Mar 21.
The intrinsic ability of vascular smooth muscle cells (VSMCs) within arterial resistance vessels to respectively contract and relax in response to elevation and reduction of intravascular pressure is essential for appropriate blood flow autoregulation. This fundamental mechanism, referred to as the myogenic response, is dependent on apposite control of myosin regulatory light chain (LC(20)) phosphorylation, a prerequisite for force generation, through the coordinated activity of myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP). Here, we highlight the molecular basis of the smooth muscle contractile mechanism and review the regulatory pathways demonstrated to participate in the control of LC(20) phosphorylation in the myogenic response, with a focus on the Ca(2+)-dependent and Rho-associated kinase (ROK)-mediated regulation of MLCK and MLCP, respectively.
动脉阻力血管中的血管平滑肌细胞（VSMCs）对血管内压力升高和降低分别作出收缩和舒张反应的内在能力对于适当的血流自动调节至关重要。这种基本机制被称为“自律反应”，依赖于肌球蛋白调节轻链（LC（20））磷酸化的适当控制，这是产生力的前提，通过肌球蛋白轻链激酶（MLCK）和肌球蛋白轻链磷酸酶（MLCP）的协调活动。在这里，我们强调了平滑肌收缩机制的分子基础，并回顾了参与自律反应中 LC（20）磷酸化控制的调节途径，重点关注 Ca（2+）依赖性和 Rho 相关激酶（ROK）介导的 MLCK 和 MLCP 的调节。
