细胞外基质的力学特性改变平滑肌蛋白LPP及其伴侣桩蛋白的表达；与早期动脉粥样硬化和血管损伤的关系。
Mechanical properties of the extracellular matrix alter expression of smooth muscle protein LPP and its partner palladin; relationship to early atherosclerosis and vascular injury.
作者信息
Jin Li, Hastings Nicole E, Blackman Brett R, Somlyo Avril V
机构信息
Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA 22908, USA.
出版信息
J Muscle Res Cell Motil. 2009;30(1-2):41-55. doi: 10.1007/s10974-009-9173-1. Epub 2009 Feb 10.
Abstract
Lipoma preferred partner (LPP) localizes to focal adhesions/dense bodies, is selectively expressed in smooth muscle cells (SMC) and enhances cell migration. SMCs cultured on denatured collagen or on a rigid substrate, up regulated expression of LPP, its partner palladin, tenascin C (TN-C), phosphorylated focal adhesion kinase (pFAK) and exhibited robust stress fibers. In an endothelial (EC)/SMC hemodynamic flow system, shear stress waveforms mimicking atheroprone flow, applied to the EC layer, significantly decreased expression of SMC LPP and palladin. They were also down regulated with TN-C, in an ApoE murine model of atherosclerosis and with oxidative stress but up regulated in an arterial injury model in response to upstream sequential changes in pFAK, Prx1 and TN-C. In conclusion, expression of LPP and palladin are modulated by a mix of mechanical cues, oxidative stress and substrate composition which translate into their up or down regulation in vessel wall injury and early atherogenesis.
摘要
脂肪瘤优先结合蛋白（LPP）定位于粘着斑/致密体，在平滑肌细胞（SMC）中选择性表达并促进细胞迁移。在变性胶原蛋白或刚性基质上培养的平滑肌细胞，LPP及其结合蛋白桩蛋白、腱生蛋白C（TN-C）、磷酸化粘着斑激酶（pFAK）的表达上调，并呈现出粗壮的应力纤维。在内皮细胞（EC）/平滑肌细胞血流动力学系统中，施加于EC层的模拟易发生动脉粥样硬化血流的切应力波形，显著降低了SMC中LPP和桩蛋白的表达。在动脉粥样硬化的载脂蛋白E小鼠模型中，它们也随TN-C下调，在氧化应激时也下调，但在动脉损伤模型中，响应pFAK、Prx1和TN-C的上游顺序变化而上调。总之，LPP和桩蛋白的表达受机械信号、氧化应激和底物成分的综合调节，这些因素在血管壁损伤和早期动脉粥样硬化发生过程中导致它们的上调或下调。
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