Bunce L A, Sporn L A, Francis C W
Department of Medicine, University of Rochester School of Medicine & Dentistry, New York 14642.
J Clin Invest. 1992 Mar;89(3):842-50. doi: 10.1172/JCI115663.
Adhesion and spreading of cultured human umbilical vein endothelial cells on fibrin surfaces of varying structure were characterized to understand better the interactions occurring between endothelium and fibrin at sites of vascular injury. Fibrin prepared with reptilase, which cleaves only fibrinopeptide A from fibrinogen, and fibrin prepared with thrombin, which cleaves both fibrinopeptide A and fibrinopeptide B, equally supported endothelial cell adhesion. In contrast, only fibrin made with thrombin mediated endothelial cell spreading, as assessed by fluorescence microscopy of cells stained with rhodamine phalloidin to identify actin stress fibers or by scanning electron microscopy. Fibrin prepared with reptilase failed to support cell spreading. To further investigate the role of the amino terminus of the fibrin beta chain after fibrinopeptide B cleavage in promoting cell spreading, protease III from Crotalus atrox venom was used to specifically cleave the amino-terminal 42 residues of the fibrinogen B beta chain. After clotting with thrombin, this fibrin derivative lacking B beta 1-42 failed to support significant cell spreading. Spreading on fibrin was unaffected by depletion of Weibel-Palade bodies from endothelial cells, indicating that the spreading was independent of stimulated von Willebrand factor release. We conclude that endothelial cell spreading on fibrin requires fibrinopeptide B cleavage and involves residues 15-42 of the fibrin beta chain.
为了更好地理解血管损伤部位内皮细胞与纤维蛋白之间的相互作用,对培养的人脐静脉内皮细胞在不同结构纤维蛋白表面的黏附与铺展特性进行了研究。用仅从纤维蛋白原切割纤维蛋白肽A的蛇毒凝血酶制备的纤维蛋白,以及用切割纤维蛋白肽A和纤维蛋白肽B的凝血酶制备的纤维蛋白,均同样支持内皮细胞黏附。相比之下,如通过用罗丹明鬼笔环肽染色以识别肌动蛋白应力纤维的细胞荧光显微镜检查或扫描电子显微镜评估,只有用凝血酶制备的纤维蛋白介导内皮细胞铺展。用蛇毒凝血酶制备的纤维蛋白不能支持细胞铺展。为了进一步研究纤维蛋白肽B切割后纤维蛋白β链氨基末端在促进细胞铺展中的作用,使用了来自锯鳞蝰蛇毒液的蛋白酶III特异性切割纤维蛋白原Bβ链的氨基末端42个残基。用凝血酶凝血后,这种缺乏Bβ1 - 42的纤维蛋白衍生物不能支持显著的细胞铺展。内皮细胞在纤维蛋白上的铺展不受内皮细胞中魏尔-帕拉德小体耗竭的影响,表明铺展与刺激的血管性血友病因子释放无关。我们得出结论,内皮细胞在纤维蛋白上的铺展需要纤维蛋白肽B切割,并且涉及纤维蛋白β链的15 - 42位残基。