Mechanotransduction in endothelial cells: temporal signaling events in response to shear stress.
Mechanotransduction in endothelial cells: temporal signaling events in response to shear stress.
复制标题
内皮细胞中的机械转导：响应剪切应力的时间信号事件。
DOI：
10.1159/000159225
复制
发表时间：
1997
影响因子：
1.7
通讯作者：
Berk,BC
中科院分区：
文献类型：
--
作者：
Takahashi,M;Ishida,T;Traub,O;Corson,MA;Berk,BC
流体剪应力是作用于血管内皮细胞的最重要的机械力之一，因为它位于血流和血管壁的交界处。最近的证据表明，几个细胞内信号事件在内皮细胞中被刺激以响应剪切力。通过这些事件，剪应力调节内皮细胞功能和血管结构，但剪应力机械转导的分子基础仍有待阐明。在我们的研究中，我们重点研究了三种对剪切力的时间信号响应：(1)作为即时反应的一氧化氮(NO)的产生；(2)作为快速反应的细胞外调节蛋白(ERK1/2；p44/p42丝裂原激活蛋白(MAP)激酶)的激活；(3)作为持续反应的粘着斑激酶(FAK)的酪氨酸磷酸化。在血管生物学方面，NO的产生、ERK1/2和FAK的激活似乎分别与血管内稳态、基因表达和细胞骨架重排有关。在这篇综述中，我们讨论了建立剪应力刺激反应的时间顺序的机制，基于信号转导分子在细胞膜上组装的层次结构。
Fluid shear stress is one of the most important mechanical forces acting upon vascular endothelium, because of its location at the interface between the bloodstream and vascular wall. Recent evidence indicates that several intracellular signaling events are stimulated in endothelial cells in response to shear stress. Through these events, shear stress modulates endothelial cell function and vascular structure, but the molecular basis of shear stress mechanotransduction remains to be elucidated. In our research we have focused on three temporal signal responses to shear stress: (1) production of nitric oxide (NO) as an immediate response; (2) activation of extracellular-regulated kinases (ERK1/2; p44/p42 mitogen-activated protein (MAP) kinases) as a rapid response, and (3) tyrosine phosphorylation of focal adhesion kinase (FAK) as a sustained response. In terms of vessel biology, NO production, and ERK1/2 and FAK activation seem to be correlated with vascular homeostasis, gene expression and cytoskeletal rearrangement, respectively. In this review, we discuss the mechanisms that establish the temporal order of shear stress-stimulated responses based on a hierarchy for assembly of signal transduction molecules at the cell plasma membrane.