PAR-triggered ERK phosphorylation in dermal (A) and lung (B) endothelial cells. Cultures were stimulated with buffer alone, PAR4 agonist (AYPGKF; 500 μM), α-thrombin (Th; 0.3 nM and 10 nM), and PAR2 agonist (SLIGRL; 100 μM) for 5 minutes. Whole-cell lysates were analyzed by immunoblot for phosphorylated ERK1/2 and total ERK1/2. Representative immunoblots are shown. Bar graphs show the mean (± SE) fold increase in ERK phosphorylation over control from 3 independent experiments. Blots were scanned and quantitated by NIH image, and data are expressed as the ratio of phosphorylated to total ERK1/2 normalized to that of control. In all experiments, the PAR2 agonist SLIGRL triggered comparable increases in ERK phosphorylation (average, approximately 5-fold) regardless of genotype.