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[血小板及血小板衍生微泡的结构表征]

[STRUCTURAL CHARACTERIZATION OF PLATELETS AND PLATELET-DERIVED MICROVESICLES].

作者信息

Ponomareva A A, Nevzorova T A, Mordakhanova E R, Andrianova I A, Litvinov R I

出版信息

Tsitologiia. 2016;58(2):105-14.

Abstract

Platelets are the anucleated blood cells, wich together with the fibrin stop bleeding (hemostasis). Cellular microvesicles are membrane-surrounded microparticles released into extracellular space upon activation and/or apoptosis of various cells. Platelet-derived macrovesicles from the major population of circulating blood microparticles that play an important role in hemostasis and thrombosis. Despite numerous studies on the pathophysiology of platelet-derived macrovesicles, mechanisms of their formation and structural details remain poorly understood. Here we investigated the ultrastructure of parental platelets and platelet-derived microvesicles formed in vitro by quiescent cells as well as by cells stimulated with one of the following activators: arachidonic acid, ADP, thrombin, calcium ionophore A23187. Using transmission electron microscopy of human platelets and isolated microvesicles, we analyzed the intracellular origin, steps of formation, structural diversity, and size distributions of the subcellular particles. We have revealed that thrombin, unlike other stimuli, not only induced vesiculation of the plasma membrane but also caused break-up of the cells followed by formation of microparticles that are comparable with microvesicles by size. A fraction of these microparticles contained cellular organelles surrounded by a thin membrane. The size of platelet-derived macrovesicles varied from 30 nm to 500 nm, however, the size distributions depended on the nature of a cell-activating stimulus. The results obtained provide new information about the formation of platelet-derived macrovesicles and their structural diversity, wich is important to understand their multiple functions in normal and disease states.

摘要

血小板是无核血细胞,与纤维蛋白一起阻止出血(止血)。细胞微泡是在各种细胞激活和/或凋亡时释放到细胞外空间的膜包被微粒。血小板衍生的大泡是循环血液中微粒的主要组成部分,在止血和血栓形成中起重要作用。尽管对血小板衍生大泡的病理生理学进行了大量研究,但其形成机制和结构细节仍知之甚少。在这里,我们研究了静止细胞以及用以下激活剂之一刺激的细胞在体外形成的亲代血小板和血小板衍生微泡的超微结构:花生四烯酸、ADP、凝血酶、钙离子载体A23187。通过对人血小板和分离的微泡进行透射电子显微镜观察,我们分析了亚细胞颗粒的细胞内起源、形成步骤、结构多样性和大小分布。我们发现,与其他刺激不同,凝血酶不仅诱导质膜形成囊泡,还导致细胞破裂,随后形成大小与微泡相当的微粒。这些微粒中的一部分含有被薄膜包围的细胞器。血小板衍生大泡的大小从30纳米到500纳米不等,然而,大小分布取决于细胞激活刺激的性质。获得的结果提供了关于血小板衍生大泡形成及其结构多样性的新信息,这对于理解它们在正常和疾病状态下的多种功能很重要。

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