Doeuvre Loïc, Angles-Cano Eduardo
Inserm U919, Sérine Protéases et Physiopathologie de l'Unité neurovasculaire, CiNaps, UMR CNRS 6232, GIP Cyceron, boulevard Henri Becquerel, 14074 Caen Cedex, France.
Med Sci (Paris). 2009 Jan;25(1):37-44. doi: 10.1051/medsci/200925137.
Cell-derived microparticles (MP) are membrane microvesicles, 0.1-1 microm in size, shed by cells following activation or during apoptosis in a variety of pathological conditions. MPs released by blood cells or by vascular endothelial cells display molecular signatures that allow their identification and functional characterization. In addition, they provide tissue factor (TF) and a procoagulant phospholipid surface. Therefore, at present, the most strongly established applied research on MPs is their procoagulant activity as a determinant of thrombotic risk in various clinical conditions. Previous studies have indicated that MPs derived from malignant cells express matrix metalloproteinases, urokinase and its receptor (uPA/uPAR) that, in the presence of plasminogen, may act in concert to degrade extracellular matrix proteins. Recently, it was shown that MPs from TNFa-stimulated endothelial cells served as a surface for interaction with plasminogen and its conversion into plasmin by the uPA/uPAR system expressed at their surface. This capacity of MPs to promote plasmin generation confers them a new profibrinolytic and proteolytic function that may be of relevance in fibrinolysis, cell migration, angiogenesis, dissemination of malignant cells, cell detachment and apoptosis.
细胞衍生的微粒（MP）是大小为0.1 - 1微米的膜微泡，在各种病理条件下，细胞在激活后或凋亡期间脱落。血细胞或血管内皮细胞释放的MP显示出可用于其鉴定和功能表征的分子特征。此外，它们提供组织因子（TF）和促凝磷脂表面。因此，目前，关于MP最确凿的应用研究是其促凝活性作为各种临床情况下血栓形成风险的决定因素。先前的研究表明，源自恶性细胞的MP表达基质金属蛋白酶、尿激酶及其受体（uPA/uPAR），在纤溶酶原存在的情况下，它们可能协同作用降解细胞外基质蛋白。最近，研究表明，来自TNFα刺激的内皮细胞的MP作为与纤溶酶原相互作用的表面，并通过其表面表达的uPA/uPAR系统将其转化为纤溶酶。MP促进纤溶酶生成的这种能力赋予它们一种新的纤溶和蛋白水解功能，这可能与纤维蛋白溶解、细胞迁移、血管生成、恶性细胞扩散、细胞脱离和凋亡有关。
