Impact of Endothelial Microparticles on Coagulation, Inflammation, and Angiogenesis in Age-Related Vascular Diseases

Figure 1

Differences in antigen expression of EMPs derived from activation versus apoptosis of endothelial cells. Endothelial cell activators, angiotensin II (Ang II), apoliprotein E (ApoE), T-cadherin (T-Cad), plasminogen activator inhibitor-1 (PAI-1), and thrombin, cause cytosolic calcium increase which leads to endothelial cell membrane disruption. Caspase-2 activates ROCK-II independently of cell death [45]. Apoptosis inducers including Rho activated kinase (ROCK-I), caspases, and FAS ligand activate caspases and cause membrane disruption in endothelial cells. Both activators of cell activation and apoptosis lead to vesiculation and EMP generation. Bars represent level of antigen on the surface of the EMP. 4 bars: high level of antigen; 1 bar: low level of antigen. EMP antigens: E-selectin, intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), platelet cell adhesion molecule-1 (PECAM-1), endoglin, vascular endothelial-cadherin (VE-cadherin), tissue factor (TF), phospholipid (PS), and von Willebrand factor (vWf). This figure was prepared based on [13, 37–40, 42, 45].