Microparticles derived from endothelial progenitor cells in patients at different cardiovascular risk.

Exposure to cardiovascular risk factors causes the release of pro-atherogenic microparticles from vascular cells and reduces the number of the atheroprotective endothelial progenitor cells (EPCs). We investigated whether microparticles shedding from EPCs are detectable in cultures of EPCs and in the circulation of subjects with various degrees of cardiovascular risk. We also investigated the relationship of EPCs-derived microparticles to cardiovascular risk factors and aortic stiffness, a marker of cardiovascular risk and impaired vascular repair by EPCs.We estimated the 10-year Framingham risk score in 105 individuals with various degrees of cardiovascular risk and measured the number of circulating EPCs, EPCs-derived microparticles (CD34+/KDR+) and aortic stiffness. Release of CD34+/KDR+ microparticles was tested in cultures of EPCs exposed to hydrogen-peroxide. CD34+/KDR+ microparticles were found in EPCs cultures incubated with hydrogen-peroxide. Framingham risk was associated with EPCs (r=-0.47, p<0.001) and CD34+/KDR+ microparticles (r=0.56, p<0.001). Low EPCs (r=-0.59, p<0.001) and high CD34+/KDR+ microparticle (r=0.57, p<0.001) levels were predictors of aortic stiffness, independent of the Framingham risk.EPCs undergo fragmentation into microparticles when exposed to a pro-apoptotic milieu. Increased microparticle shedding from EPCs may reduce circulating EPCs levels and may thus contribute to increase aortic stiffness beside traditional risk factors.