Martinsen A, Dessy C, Morel N
a Cell physiology; IoNS; UCLouvain ; Brussels , Belgium.
Channels (Austin). 2014;8(5):402-13. doi: 10.4161/19336950.2014.950537.
Smooth muscle myosin light chain kinase (MLCK) plays a crucial role in artery contraction, which regulates blood pressure and blood flow distribution. In addition to this role, MLCK contributes to Ca(2+) flux regulation in vascular smooth muscle (VSM) and in non-muscle cells, where cytoskeleton has been suggested to help Ca(2+) channels trafficking. This conclusion is based on the use of pharmacological inhibitors of MLCK and molecular and cellular techniques developed to down-regulate the enzyme. Dissimilarities have been observed between cells and whole tissues, as well as between large conductance and small resistance arteries. A differential expression in MLCK and ion channels (either voltage-dependent Ca(2+) channels or non-selective cationic channels) could account for these observations, and is in line with the functional properties of the arteries. A potential involvement of MLCK in the pathways modulating Ca(2+) entry in VSM is described in the present review.
平滑肌肌球蛋白轻链激酶(MLCK)在动脉收缩中起关键作用,动脉收缩调节血压和血流分布。除了这一作用外,MLCK还参与血管平滑肌(VSM)和非肌肉细胞中的Ca(2+)通量调节,在这些细胞中,细胞骨架被认为有助于Ca(2+)通道的运输。这一结论是基于使用MLCK的药理学抑制剂以及为下调该酶而开发的分子和细胞技术得出的。在细胞与整个组织之间以及大电导和小阻力动脉之间均观察到差异。MLCK和离子通道(电压依赖性Ca(2+)通道或非选择性阳离子通道)的差异表达可以解释这些观察结果,并且与动脉的功能特性一致。本综述描述了MLCK在调节VSM中Ca(2+)内流途径中的潜在作用。