Figure 2.

Mechanisms involved in endothelial damage and repair. Upon activation endothelial cells express adhesion molecules (i.e.; VCAM-1 and ICAM-1), which allow leukocytes to adhere, transmigrate, and initiate a cascade of inflammatory reactions and the release of EMP into the circulation. With significant endothelial damage, cells become senescent and are detached. This ultimately leads to the recruitment of CAC, monocyte-macrophage-derived cells that contribute to vascular repair by adhering to loci of endothelial damage, and producing angiogenic cytokines that induce the mobilization of EPC from the bone marrow. The angiogenic cytokines produced by CAC also serve as homing molecules with a chemotactic effect on EPC. As a consequence, EPC migrate to damaged endothelium and eventually integrate into the endothelial cell layer. Besides being released after endothelial activation, EMPs also contributes to endothelial homeostasis by cytoprotective effects on endothelial cells, including reduced apoptosis. EC, Endothelial Cell; VSMC, Vascular Smooth Muscle Cell; VCAM-1, Vascular Cell Adhesion Molecule 1; ICAM-1, InterCellular Adhesion Molecule 1; EMP, Endothelial MicroParticles; CAC, Circulating Angiogenic Cells; EPC, Endothelial Progenitor Cells.