The role of microparticles in chronic obstructive pulmonary disease.

Abstract

Accumulating evidence suggests that cell injury in lung tissues is closely connected to disease progression in chronic obstructive pulmonary disease (COPD). Microparticles (MPs) are shed membrane vesicles that are released from platelets, leukocytes, red blood cells, and endothelial cells when these cells are activated or undergo apoptosis under inflammatory conditions. Based on increasing evidence that endothelial injury in the pulmonary capillary vasculature leads to lung destruction, and because cardiovascular diseases are the main cause of death among individuals with COPD, endothelial MPs (EMPs) are now receiving attention as potential biomarkers for COPD. There are eight types of EMPs which are defined by the presence of different endothelial markers on the cell membrane: vascular endothelial-cadherin; platelet endothelial cell adhesion molecule; melanoma cell adhesion molecule; E-selectin; CD51; CD105; von Willebrand factor; and CD143 EMPs. Vascular endothelial-cadherin, platelet endothelial cell adhesion molecule, and E-selectin EMPs are increased in patients with stable COPD and are further increased in patients with exacerbated COPD compared to non-COPD patients. In addition, the levels of these three EMPs in patients with stable COPD are significantly correlated with lung destruction and airflow limitation. These results indicate that endothelial injury is closely connected to the pathophysiology of COPD. Interestingly, the variations in the levels of the eight EMP subtypes were not identical with changes in patient condition. Although the clinical significance of the differences in these eight EMP subtypes remains unclear, evaluating the expression pattern of endothelial antigens on circulating MPs might predict the presence and degree of endothelial injury in COPD patients. In addition, circulating MPs are proposed to have several physiological functions in vivo, such as intercellular crosstalk; the increase in EMPs in COPD seems to play a role in the pathophysiology of this disease.