Charles E. Wade,Jessica C. Cardenas

Endothelial cell integrity and function are now recognized as being important in cardiovascular health. The integrity of the endothelium is associated with a wide range of functions such as control of vasomotor activity, regulation of the coagulation system, angiogenesis, mediation of inflammation, and edema formation. Endothelial dysfunction has been implicated in the pathophysiology of numerous cardiovascular diseases. Thus, assessing endothelial dysfunction or damage is important in understanding a patient’s clinical course and in developing new potential interventions.

Currently, evaluating the contribution of the endothelium to disease processes clinically has been complicated by the absence of adequate methods to qualify endothelial homeostasis. Recent work suggests that an increase in circulating endothelial microparticles is indicative of damage to the endothelium. Microparticles are submicron-size vesicles that are formed by budding from the cell membrane and usually carry cytoplasmic constituents such as proteins, bioactive lipids, and genetic material. Microparticles exhibit distinct features of their parent cells and can perform similar biological functions. Endothelial-derived microparticles (EMPs), in particular, participate in hemostasis by supporting coagulation and fibrinolysis. The formation of microparticles is thought to be associated with endothelial activation or apoptosis. Increases in EMP release have been documented during a number of disease processes. In contrast, endothelial progenitor cells (EPCs) are associated with endothelial repair after damage. EPCs are produced by the bone marrow and differentiate into mature endothelial cells upon encountering sites of vascular endothelial denudation. A reduction in EPC numbers is associated with endothelial repair by acute formation of a cellular patch at the site of injury resulting in a reduction in the number of circulating cells.