Pirro Matteo, Schillaci Giuseppe, Paltriccia Rita, Bagaglia Francesco, Menecali Cinzia, Mannarino Massimo R, Capanni Marusca, Velardi Andrea, Mannarino Elmo
Department of Clinical and Experimental Medicine, University of Perugia, Italy.
Arterioscler Thromb Vasc Biol. 2006 Nov;26(11):2530-5. doi: 10.1161/01.ATV.0000243941.72375.15. Epub 2006 Aug 31.
Atherosclerosis may be caused by increased endothelial damage and by a consumptive loss of endothelial repair capacity by endothelial progenitors. Arterial stiffness is a reliable marker of atherosclerosis and a positive correlate of endothelial damage. We investigated whether an increased ratio of CD31+/CD42- microparticles to endothelial progenitors, a possible indicator of endothelial damage and impaired endothelium reparation, may contribute to aortic stiffness in hypercholesterolemia. We also studied the in vitro effect of microparticles from hypercholesterolemic patients on endothelial progenitor survival.
Circulating CD31+/CD42- microparticles, endothelial progenitors, and aortic pulse wave velocity (aPWV), a measure of aortic stiffness, were measured in 50 patients with never-treated hypercholesterolemia and 50 normocholesterolemic controls. Hypercholesterolemic patients had more circulating CD31+/CD42- microparticles, less endothelial progenitors, and a stiffer aorta than controls. aPWV was associated with CD31+/CD42- microparticles (r=0.61; P<0.001), endothelial progenitors (r=-0.45, P<0.001), and with cholesterol levels (r=0.51; P<0.001). High plasma cholesterol and a high ratio of CD31+/CD42- microparticles to endothelial progenitors independently predicted an increased aPWV. Microparticles from hypercholesterolemic patients caused a significant endothelial progenitor loss in vitro.
Hypercholesterolemia-related aortic stiffness is promoted by plasma cholesterol directly, increased endothelial damage, and reduced endothelium repair capacity by endothelial progenitors.
动脉粥样硬化可能是由于内皮损伤增加以及内皮祖细胞对内皮修复能力的消耗性丧失所致。动脉僵硬度是动脉粥样硬化的可靠标志物，也是内皮损伤的正相关指标。我们研究了CD31+/CD42-微粒与内皮祖细胞的比例增加（这可能是内皮损伤和内皮修复受损的一个指标）是否会导致高胆固醇血症患者的主动脉僵硬度增加。我们还研究了高胆固醇血症患者的微粒对内皮祖细胞存活的体外影响。
在50例未经治疗的高胆固醇血症患者和50例正常胆固醇血症对照者中，测量了循环中的CD31+/CD42-微粒、内皮祖细胞以及主动脉脉搏波速度（aPWV，一种主动脉僵硬度的测量指标）。高胆固醇血症患者的循环CD31+/CD42-微粒更多，内皮祖细胞更少，且主动脉比对照组更僵硬。aPWV与CD31+/CD42-微粒（r = 0.61；P < 0.001）、内皮祖细胞（r = -0.45，P < 0.001）以及胆固醇水平（r = 0.51；P < 0.001）相关。高血浆胆固醇以及CD31+/CD42-微粒与内皮祖细胞的高比例独立预测了aPWV的增加。高胆固醇血症患者的微粒在体外导致了显著的内皮祖细胞损失。
高胆固醇血症相关的主动脉僵硬度是由血浆胆固醇直接促进的，同时伴有内皮损伤增加以及内皮祖细胞对内皮修复能力的降低。
