原纤蛋白-1片段的固定化增强了聚四氟乙烯的生物相容性。

Immobilisation of a fibrillin-1 fragment enhances the biocompatibility of PTFE.

作者信息

Hajian Hamid, Wise Steven G, Bax Daniel V, Kondyurin Alexey, Waterhouse Anna, Dunn Louise L, Kielty Cay M, Yu Young, Weiss Anthony S, Bilek Marcela M M, Bannon Paul G, Ng Martin K C

机构信息

Heart Research Institute, Sydney, NSW 2042, Australia; The Baird Institute, Sydney, NSW 2042, Australia.

Heart Research Institute, Sydney, NSW 2042, Australia; Sydney Medical School, University of Sydney, NSW 2006, Australia; School of Molecular Bioscience, University of Sydney, NSW 2006, Australia.

出版信息

Colloids Surf B Biointerfaces. 2014 Apr 1;116:544-52. doi: 10.1016/j.colsurfb.2014.01.042. Epub 2014 Feb 4.

DOI:10.1016/j.colsurfb.2014.01.042

PMID:24572497

Abstract

Current vascular biomaterials exhibit poor biocompatibility characterised by failure to promote endothelialisation, predisposition to neoinitmal hyperplasia and excessive thrombogenicity. Fibrillin-1, a major constituent of microfibrils is associated with elastic fibres in the arterial wall. Fibrillin-1 binds to endothelial cells through an RGD cell adhesion motif in the fourth TB module. The RGD motif is present in PF8, a recombinant fibrillin-1 fragment. We investigated the potential of PF8 to improve the biocompatibility of PTFE. PF8 enhanced endothelial cell attachment and cell proliferation to a greater extent than fibronectin (p<0.01). PF8 immobilised on PTFE using plasma immersion ion implantation (PIII), retained these favourable cell interactive properties, again promoting endothelial cell attachment and proliferation. The thrombogenicity of covalently bound PF8 on PTFE was assessed in both static and dynamic conditions. In static conditions, uncoated PIII treated PTFE was more thrombogenic than untreated PTFE, while PF8 coating reduced thrombogenicity. Under flow, there was no difference in the thrombogenicity of PF8 coated PTFE and untreated PTFE. Immobilised PF8 shows a striking ability to promote attachment and growth of endothelial cells on PTFE, while providing a non-thrombogenic surface. These features make PF8 a promising candidate to improve the biocompatibility of current synthetic vascular grafts.

摘要

目前的血管生物材料表现出较差的生物相容性，其特征为无法促进内皮化、易于发生新生内膜增生以及具有过高的血栓形成倾向。原纤维蛋白-1是微原纤维的主要成分，与动脉壁中的弹性纤维相关。原纤维蛋白-1通过第四个TB模块中的RGD细胞黏附基序与内皮细胞结合。RGD基序存在于重组原纤维蛋白-1片段PF8中。我们研究了PF8改善聚四氟乙烯生物相容性的潜力。与纤连蛋白相比，PF8在更大程度上增强了内皮细胞的黏附和细胞增殖（p<0.01）。使用等离子体浸没离子注入（PIII）将PF8固定在聚四氟乙烯上，保留了这些有利的细胞相互作用特性，再次促进了内皮细胞的黏附和增殖。在静态和动态条件下评估了共价结合在聚四氟乙烯上的PF8的血栓形成性。在静态条件下，未涂层的经PIII处理的聚四氟乙烯比未处理的聚四氟乙烯具有更高的血栓形成性，而PF8涂层降低了血栓形成性。在流动条件下，PF8涂层的聚四氟乙烯和未处理的聚四氟乙烯的血栓形成性没有差异。固定化的PF8显示出显著的能力，可促进内皮细胞在聚四氟乙烯上的黏附和生长，同时提供非血栓形成表面。这些特性使PF8成为改善当前合成血管移植物生物相容性的有希望的候选者。