Morgenstern E, Edelmann L, Reimers H J, Miyashita C, Haurand M
Eur J Cell Biol. 1985 Sep;38(2):292-300.
The fibrinogen distribution in platelet organelles after ADP-stimulation was investigated with anti-human fibrinogen using protein A-gold applied to serial sections. Fibrinogen was detected in the so-called alpha-granules of platelets and also in granule protrusions which were observed after ADP-stimulation. The ends of these protrusions were formed as coated membranes and the tips were often in apposition to the surface connected membranes or the plasmalemma. At such places fusion events and hence signs of an exocytosis could be demonstrated by means of cryofixation and cryosubstitution. Examination of serial sections revealed fibrinogen on all these granule profiles. Surface connected membranes, free surfaces and the characteristic structure of the contact zones of aggregated platelets were also labelled by gold particles but less than anticipated. On the platelet surfaces and surface connected membranes fibrinogen was rarely demonstrable with ferritin-labelled anti-human fibrinogen on washed or thrombin-stimulated, almost fibrinogen free platelets. After addition of human fibrinogen to the thrombin stimulated and disaggregated platelets a part of the platelets aggregated spontaneously and formed characteristic contact zones. Anti-human fibrinogen was observed on the free surfaces, in filamentous bridges between the contact spaces and in a tubular surface connected membrane system with involvement of coated membranes at the central ends of these structures. The results indicate the following: all alpha-granules contain fibrinogen; after ADP-stimulation secretion takes place with involvement of coated membranes; during aggregation fibrinogen binds to platelet surfaces and forms contact spaces; fibrinogen is taken up by the surface connected system with involvement of coated membranes.
利用抗人纤维蛋白原，通过将蛋白A-金应用于连续切片，研究了ADP刺激后血小板细胞器中纤维蛋白原的分布。在血小板所谓的α颗粒中以及在ADP刺激后观察到的颗粒突起中均检测到纤维蛋白原。这些突起的末端形成被膜，其尖端常常与表面连接膜或质膜并置。在这些部位，通过冷冻固定和冷冻置换可证实融合事件以及因此而产生的胞吐迹象。连续切片检查显示所有这些颗粒轮廓上均有纤维蛋白原。表面连接膜、游离表面以及聚集血小板接触区的特征性结构也被金颗粒标记，但比预期的要少。在洗涤过的或经凝血酶刺激的、几乎不含纤维蛋白原的血小板上，用铁蛋白标记的抗人纤维蛋白原很难在血小板表面和表面连接膜上证实有纤维蛋白原。向经凝血酶刺激并解聚的血小板中加入人纤维蛋白原后，一部分血小板自发聚集并形成特征性接触区。在游离表面、接触间隙之间的丝状桥以及一个管状表面连接膜系统中观察到抗人纤维蛋白原，这些结构的中央末端有被膜参与。结果表明：所有α颗粒均含有纤维蛋白原；ADP刺激后，在被膜参与下发生分泌；聚集过程中，纤维蛋白原与血小板表面结合并形成接触间隙；纤维蛋白原通过被膜参与的表面连接系统被摄取。
