Platelet endothelial cell adhesion molecule-1 and mechanotransduction in vascular endothelial cells

被引:71
作者
Fujiwara, K [1 ]
机构
[1] Univ Rochester, Med Ctr, Inst Cardiovasc Res, Rochester, NY 14642 USA
关键词
ERK; fluid shear stress; mechanosignal transduction; PECAM-1; SHP-2;
D O I
10.1111/j.1365-2796.2006.01623.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Endothelial cells are known to respond to mechanical forces such as fluid shear stress and cyclic stretch, but elucidating the mechanism for mechanosensing has been difficult. Experimental data indicate that there are probably several sensing mechanisms. We have recently proposed a novel mechanoresponse mechanism that involves platelet endothelial cell adhesion molecule-1 (PECAM-1). When endothelial cells are stimulated by fluid shear stress, PECAM-1 is tyrosine phosphorylated and activates the extracellular signal-regulated kinase 1 and 2 (ERK1/2) signalling cascade. The same signalling events occurred when we applied pulling force directly on PECAM-1 on the endothelial cell surface using magnetic beads coated with antibodies against the external domain of PECAM-1. These results appear to indicate that PECAM-1 is a mechanotransduction molecule. To our knowledge, this is the first mammalian molecule that is shown to respond to mechanical force directly exerted to it.
引用
收藏
页码:373 / 380
页数:8
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