Diabetes induces proangiogenic response which is characterized by fragile blood vessels. Advanced glycation end products (AGEs) accumulating under hyperglycemic conditions are acknowledged to play a causative role in the vascular complications of diabetes including retinopathy associated with excessive angiogenesis. However, the detailed mechanism of AGEs-mediated excessive angiogenesis is poorly understood. Therefore, we elucidate one part of this mechanism. Matrigel tube formation assay was performed using the mouse endothelial cell line, b.End5 cells. The areas and total lengths of the tubes were calculated as the degree of tube formation. Uptake of AGEs by b.End5 cells were measured using flow cytometry. pNFκB/NFκB ratio were analyzed by western blot. AGE2 and AGE3 concentration-dependently increased the area and length of tubular structures. Uptake of AGE2 and AGE3 by b.End5 cells concentration-dependently was increased. AGE2 and AGE3 activated NFκB. Induction of tube formation by AGE2/3 and AGE2/3 uptake by b.End5 cells were significantly suppressed by pinocytosis inhibitor, EIPA, or NFκB inhibitor, PDTC. Our results indicate that AGEs uptake by b.End5 cells may be mediated by pinocytosis. Moreover, pinocytosis of AGEs may induce phosphorylation of NFκB in endothelial cells, and then promote angiogenesis.