ABSTRACT
In the body, vascular endothelial cells (ECs) are constantly exposed to shear stress, which is the tangential component of hemodynamic forces acting on the vessel wall. While shear stress plays important roles in maintaining vascular homeostasis, it can also be pathophysiological factors in vascular disorders such as atherosclerosis. Flow channels with cultured ECs such as human umbilical vein endothelial cells (HUVECs) and bovine aortic endothelial cells (BAECs) have been used as in vitro models to study the endothelial responses to applied shear stress. Such studies have demonstrated that the application of shear stress leads to the phosphorylation of multiple cellular proteins in ECs, resulting in the activation of signaling pathways to modulate gene
expression, cytoskeletal organization, vessel dilation/constriction, and cell proliferation/ apoptosis. These phosphorylation cascades have been shown to result from the activation of cellular pr otein tyrosine kinases (PTKs) and Ser/Thr kinases.
