A long term goal of my laboratory is to understand mechanisms by which G protein-coupled receptor (GPCR) signaling leads to vascular inflammation, atherosclerosis, and thrombosis. Two major research programs are currently under investigation. One research program focuses on the role of P2Y2 receptor, an ATP/UTP-sensitive nucleotide receptor, in promoting pro-thrombotic gene expression such as the tissue factor gene, and its participation in inflammation-induced thrombosis. A second area focuses on a chemokine receptor termed CXCR7. We are trying to understand how CXCR7 is induced during monocyte-to-macrophage differentiation and its significance in cell signaling and in promoting vascular inflammation and atherosclerosis. All research projects rely heavily on molecular biology, biochemical, and pharmacological methods in cultured vascular endothelial cells and blood monocytes/macrophages. Genetic approaches like new mouse models with endothelial cell-specific and myeloid cells-targeted deletion of the P2Y2 receptor or CXCR7 genes are also employed for in vivo study. An overriding objective of the research programs is to identify novel molecular targets for anti-inflammation therapy with a focus on cardiovascular diseases such as atherosclerosis.