LAUSR

Previously, we demonstrated that exogenous heat shock protein 27 (HSP27/gene, HSPB1) treatment of human endothelial progenitor cells (EPCs) increases the synthesis and secretion of VEGF, improves EPC‐migration/re‐endothelialization and decreases neo‐intima formation, suggesting a role for HSPB1 in regulating EPC function. We hypothesized that HSPB1 also affects mature endothelial cells (ECs) to alter EC‐mediated vasoreactivity in vivo. Our work focused on endothelial NOS (eNOS)/NO‐dependent relaxation induced by ACh and the coagulation pathway‐activated receptor, proteinase‐activated receptor 2 (PAR2).