ABSTRACT Endothelial dysfunction/apoptosis is critical to the development of neointima hyperplasia. Our pilot study identified a novel member of the caspase subfamily, caspase 13 (CASP 13), which is induced by oxidized low density lipoprotein (ox-LDL) in endothelial cells, but not in vascular smooth muscle cells. It remains controversial whether CASP 13 is a human or bovine gene. In this study, we collected four human brachial artery segments during arterioveinous fistula graft removal surgeries. By western blot and quantitative RT-PCR analysis, CASP13 expression was elevated at the anastomosis of brachial arteries from patients receiving hemodialysis. Rat carotid artery balloon model is widely used as in vivo atherosclerosis model for studies on neointima formation and especially vascular smooth muscle proliferation. However, most of the balloon injury studies terminated on the 14th day to sacrifice the animals for histological studies. In this study, we employed the ultrasonic device to record the hemodynamic changes in rat carotid artery at different time intervals after balloon injury. The pre-operative mean left carotid artery internal diameter and blood flow of Sprauge Dawley rats was 0.6 ¡Ó 0.07 mm and 28.75 ¡Ó 4.45 cm/sec, respectively. After balloon dilatation, the mean internal diameter of left carotid artery elevated to 0.77 ¡Ó 0.09 mm and 0.71 ¡Ó 0.08 mm on day 7 and day 14, respectively. Besides, the mean blood flow velocity also increased to 47.6 ¡Ó 9.2 cm/sec and 33.4 ¡Ó 10.8 cm/sec on day 7 and day 14, respectively. However, the left carotid artery blood flow velocity returned to 24 ¡Ó 3.5 cm/sec on day 21. The CASP 13 protein expression was found elevated in the balloon injury sites and mainly localized in the endothelial cells. In summary, CASP 13 is detected in endothelial cells in both human and rat atherosclerosis models and may constitute a novel molecular target for vascular diseases.