Microparticles are at least 200-fold more concentrated and generate twice as much thrombin in human atherosclerotic plaques compared to plasma.
Observational (n=26)
What are the cellular origins and thrombogenic activity of microparticles in human atherosclerotic plaques compared to plasma?
Microparticles in human atherosclerotic plaques are highly concentrated, originate primarily from leukocytes and erythrocytes, and exhibit significantly higher thrombogenic activity than plasma microparticles.
OBJECTIVES: In this study, we evaluated the cellular origins and thrombogenic potential of microparticles. BACKGROUND: Human atherosclerotic plaques contain submicron vesicles (microparticles) released during cell activation or apoptosis. METHODS: Microparticles were purified from plaques and platelet-free plasma from 26 patients undergoing carotid endarterectomy. Flow cytometry analysis revealed the presence of large amounts of microparticles in plaques but not in healthy vessels. RESULTS: Most plaque microparticles originated from leukocytes, of which 29 +/- 5% were macrophages, 15 +/- 3% lymphocytes, and 8 +/- 1% granulocytes. Plaques microparticles also derived from erythrocytes (27 +/- 4%), smooth muscle (13 +/- 4%) and endothelial cells (8 +/- 2%), but not from platelets. Plaques from asymptomatic and symptomatic patients showed no differences in microparticle origins. Microparticles were at least 200-fold more concentrated in plaque than in plasma. Plasma microparticles were primarily platelet-derived in contrast with those of plaque and showed no smooth muscle cell origin. Both plaque and plasma microparticles exposed tissue factor and generated thrombin, but this activity was twice as high in microparticles isolated from plaques, reflecting the thrombogenic contribution of the individual classes of microparticles. CONCLUSIONS: These results demonstrate that microparticles are more abundant and more thrombogenic in human atherosclerotic plaques than in plasma. The different cellular origins of plaque and plasma microparticles might explain the increased thrombogenic activity of plaque microparticles.
Leroyer et al. (Thu,) conducted a observational in Atherosclerosis (n=26). Plaque microparticles vs. Plasma microparticles was evaluated on Cellular origins and thrombogenic activity (tissue factor exposure and thrombin generation). Microparticles are at least 200-fold more concentrated and generate twice as much thrombin in human atherosclerotic plaques compared to plasma.