Background: Atherosclerotic plaque disruption and subsequent thrombosis formation is responsible for many thrombotic complications in cardiovascular disease. Tissue factor (TF) exposure upon plaque rupture can trigger thrombin formation. Thrombin, on the other hand, can induce tissue factor expression in human umbilical vein endothelial cells or saphenous vein endothelial cells. The impact of thrombin in the endothelial cells of arterial side was less known. Methods: Human aortic endothelial cells (HAEC) were cultivated and methoxyphenyl tetrazolium inner salt assays were used to determine the non-toxicity of thrombin to endothelial cells. Real-time PCR was used to determine the relative TFmRNA quantity. Western blot was used to determine the relative protein level. TF functional activity was determined by a chromogenic assay. Results: Thrombin was non-toxic to the HAEC. TF mRNA relative quantity was enhanced 390±114% by thrombin (P=0.034). TF protein relative quantity was enhanced 332±39% by thrombin (P=0.01). TF activity was enhanced 547±54% by thrombin (P＜0.001). Conclusion: Thrombin is a sufficient stress to induce TF expression in HAEC. The transcriptional control by thrombin causes an increase in TF mRNA. This increase in mRNA is modestly paralleled by an increase in protein level and functional activity.