Morphing the topography of atherosclerosis: an unexpected role for PECAM-1.

Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a complex adhesion and signaling molecule expressed by endothelial cells, platelets, and leukocytes.1,2 On endothelial cells this transmembrane glycoprotein member of the immunoglobulin gene superfamily is concentrated at intercellular junctions and cycles through vesicle-like structures contiguous with the lateral plasma membrane, termed the lateral border recycling compartment.3 Homophilic adhesive interactions between PECAM-1 on leukocytes and endothelial cells mediate leukocyte migration through endothelial cell monolayers (diapedesis) in vitro and in vivo and through the perivascular basement membrane.2,4 As a signaling molecule, PECAM-1 transduces signals required for proinflammatory adhesion molecule expression by endothelial cells. However, PECAM-1 can also inhibit inflammatory and immune responses.2 Thus, PECAM-1 has the potential to influence atherogenesis in more than one way.