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首页> 外文期刊>Cell and Tissue Research >Endothelial microparticles in diseases.
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Endothelial microparticles in diseases.

机译：疾病中的内皮微粒。

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Microparticles are submicron vesicles shed from plasma membranes in response to cell activation, injury, and/or apoptosis. The measurement of the phospholipid content (mainly phosphatidylserine; PSer) of microparticles and the detection of proteins specific for the cells from which they are derived has allowed their quantification and characterization. Microparticles of various cellular origin (platelets, leukocytes, endothelial cells) are found in the plasma of healthy subjects, and their amount increases under pathological conditions. Endothelial microparticles (EMP) not only constitute an emerging marker of endothelial dysfunction, but are also considered to play a major biological role in inflammation, vascular injury, angiogenesis, and thrombosis. Although the mechanisms leading to their in vivo formation remain obscure, the release of EMP from cultured cells can be caused in vitro by a number of cytokines and apoptotic stimuli. Recent studies indicate that EMP are able to decrease nitric-oxide-dependent vasodilation, increase arterial stiffness, promote inflammation, and initiate thrombosis at their PSer-rich membrane, which highly co-expresses tissue factor. EMP are known to be elevated in acute coronary syndromes, in severe hypertension with end organ damage, and in thrombotic thrombocytopenic purpura, all conditions associated with endothelial injury and pro-thrombotic state. The release of EMP has also been associated with endothelial dysfunction of patients with multiple sclerosis and lupus anticoagulant. More recent studies have focused on the role of low shear stress leading to endothelial cell apoptosis and subsequent EMP release in end-stage renal disease. Improved knowledge of EMP composition, their biological effects, and the mechanisms leading to their clearance will probably open new therapeutic approaches in the treatment of atherothrombosis.
机译：微粒是响应细胞活化，损伤和/或凋亡而从质膜脱落的亚微米囊泡。对微粒中磷脂含量（主要是磷脂酰丝氨酸; PSer）的测量以及对源自其的细胞特异的蛋白质的检测已经对其进行了定量和表征。在健康受试者的血浆中发现了各种细胞起源的微粒（血小板，白细胞，内皮细胞），并且它们的数量在病理条件下增加。内皮微粒（EMP）不仅构成内皮功能障碍的新兴标志物，而且还被认为在炎症，血管损伤，血管生成和血栓形成中起着重要的生物学作用。尽管导致它们在体内形成的机制仍然不清楚，但是体外培养的细胞中EMP的释放可能是由多种细胞因子和凋亡刺激物引起的。最近的研究表明，EMP能够减少一氧化氮依赖性血管舒张，增加动脉僵硬度，促进炎症并在富含PSer的膜上引发血栓形成，而PSer膜高度共表达组织因子。已知EMP在急性冠状动脉综合征，伴有终末器官损害的严重高血压，血栓性血小板减少性紫癜，与内皮损伤和血栓形成前状态相关的所有疾病中均升高。 EMP的释放也与多发性硬化和狼疮抗凝剂患者的内皮功能障碍有关。最近的研究集中在低剪切应力导致内皮细胞凋亡和随后的EMP释放在终末期肾脏疾病中的作用。对EMP组成，其生物学作用以及导致其清除的机制的认识的提高，可能会为治疗动脉粥样硬化形成新的治疗方法。

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