(A) Human aortic endothelial cells were subjected to lentiviral infection introducing full-length or DN-RAGE. Cells were exposed to S100b and permeability assay performed. *P < 0.0001 versus unstimulated full-length RAGE; **P < 0.0001 versus S100b-stimulated full-length RAGE. (B and C) Human endothelial cells were subjected to introduction of siRNA to reduce RAGE transcripts (B) and RAGE protein (C) without effect on GAPDH transcripts or protein. (D) Endothelial cells were subjected to RAGE or scramble siRNA and incubated with 10 μg/ml S100b for 4 hours. Western blotting was performed to probe VCAM-1 antigen and β-actin. *P < 0.0001. (E) Human aortic endothelial cells were stimulated with 10 μg/ml S100b for 20 minutes. Western blotting was performed to detect phospho/total-JNK MAP kinases. *P < 0.0001. (F) Endothelial cells were treated with JNK MAP kinase inhibitor SP60025 (10 μM) for 60 minutes followed by S100b (10 μg/ml) for 4 hours and Western blotting performed with anti–VCAM-1 IgG and anti–β-actin IgG. **P < 0.0001 versus S100b-stimulated, non–SP600125-treated. (G) oxLDL (5 μg/ml) was incubated with human aortic endothelial cells and Western blotting performed for detection of phospho/total-JNK MAP kinase. (H) Cells were treated with 10 μM SP600125 for 1 hour followed by incubation with oxLDL for 4 hours. Western blotting was performed for detection of VCAM-1 antigen. *P < 0.0001. (I) Cells were treated with siRNA to knock down JNK MAP kinase followed by incubation with oxLDL for 4 hours. Western blotting was performed for detection of VCAM-1 antigen. Where indicated by the white line, lanes were run on the same gel but were noncontiguous. *P < 0.05; **P < 0.01.