Our mission is to understand the role of signaling microdomains in mediating cellular communication within the vasculature, focusing on possible disregulation of these domains in disease states. We utilize novel cell biology and proteomic approaches, coupled with extensive validation in whole animal. We are especially interested in post-translational modifications of proteins that regulate 1) the mechanisms by which plasminogen activator inhibitor-1 degrades extracellular matrix and induces myoendothelial junction formation, 2) Cx43-mediated cellular proliferation in smooth muscle cells and 3) polarized activation of eNOS in the resistance vasculature.