Vascular endothelial cells (ECs) constitute the innermost lining of blood vessels and are central to vascular physiological processes. As blood flows, it exerts a frictional force on the endothelial surface. This force is expressed as shear stress on the ECs, which is defined as the product of the blood viscosity and the blood velocity gradient measured at the vessel wall. Although it is well established that shear stress affects a wide spectrum of EC functions, much of the mechanotransduction process remains to be explored. A transcription factor named Ets-1 controls the expression of many genes that encode EC specific markers or proteins involved in wound healing. It is known that ECs express high levels of Ets-1 during wound healing, whereas quiescent ECs express minimal amounts of Ets-1. It is also known that shear stress enhances wound healing. Moreover, vascular endothelial growth factor and basic fibroblast growth factor are known inducers of Ets-1 and their inductive effect is mediated by the activation of MAP kinases p38 and ERK ½, both of which can be activated by shear stress as well. Using subconfluent ECs as a wound model, herein we tested the hypothesis that shear stress may affect Ets-1 expression in a time dependent manner, i.e., upregulate Ets-1 expression at the early phase of wound healing. Briefly, ECs were cultured for 24 hours at 1/12 confluency on a glass slide pre-coated with type I collagen. Using a hydrodynamic flow system, the ECs were then subject to an arterial shear stress of 1.5 Pa for 0, 4 and 17 hours. The sheared ECs and static controls were then fluorescently stained for Ets-1. Nuclear and cytosol Ets-1 levels were measured using video-fluorescence microscopy. We found that, in static controls, Ets-1 levels decreased from 0 to 17 hours. On the contrary, Ets-1 levels in sheared ECs increased between 0-4 hours and decreased between 4-17 hours. The increase in Ets-1 protein production by shear stress supports our hypothesis that Ets-1 may mediate the shear enhancement of wound healing.