Objective    The advanced glycation end products (AGEs) play an important role in the development of atherosclerosis. Increased formation of AGEs is generally regarded as one of the main mechanisms responsible for vascular damage. Recent evidences have shown that bone marrow-derived endothelial progenitor cells (EPCs) play a pivotal role in the repair and regeneration of the damaged vessels. We aimed to explore the effect of AGEs on the biological functions of cultured EPCs.     Methods    EPCs

isolated from bone marrow

were cultured in the absence or presence of AGEs (50

100

150

200 and 400 μg/ml). A modified Boyden’s chamber was used to assess the migration of EPCs， and the number of recultured EPCs was counted to determine the cell adhesiveness. A spectrophotometer was used to determine the proliferation. Reactive oxygen species (ROS) were analyzed using the ROS assay kit. Apoptosis was evaluated by Annexin Ⅴ immunostaining.     Results    Co-culturing with AGEs inhibited the proliferation

migration and adhesion of EPCs

increased ROS production and induced cell apoptosis. In addition

these effects were attenuated when ALT711

an inhibitor of AGEs crosslinking was co-incubated.     Conclusion    AGEs mediate impairment of EPCs function

which indicates a new pathophysiological mechanism of disturbed vascular adaptation in atherosclerosis and suggests that lower levels of AGEs might improve the success of progenitor cell therapy.