Department of Biomedical Engineering, National Cerebral and Cardiovascular Center Research Institute, 6-1 Kishibe-Shimmachi, Suita, Osaka, 564-8565, Japan.
Department of Biomedical Engineering, National Cerebral and Cardiovascular Center Research Institute, 6-1 Kishibe-Shimmachi, Suita, Osaka, 564-8565, Japan.
Colloids Surf B Biointerfaces. 2020 Sep;193:111113. doi: 10.1016/j.colsurfb.2020.111113. Epub 2020 May 15.
We recently reported in vitro suppression of platelet adhesion on expanded polytetrafluoroethylene (ePTFE) by surface grafting of poly(2-methacryloyloxyethyl phosphorylcholine) (PMPC). However, this may be inadequate for long-term hemocompatibility of blood-contacting biomaterials, and it has led us to develop a strategy of circulating mononuclear cell-capture. ePTFE was treated with argon (Ar) plasma, and grafted with 2-methacryloyloxyethyl phosphorylcholine (MPC) and methacrylic acid (MAA), by glycidyl methacrylate (GMA)-anchored graft polymerization. Next, it was immobilized with integrin α4β1-positive circulating blood cell-specific peptides, i.e., the traditional arginine-glutamic acid-aspartic acid-valine (REDV), and our original hemocompatible peptide-1 (HCP-1). Both the surfaces retained the anti-platelet property just like the PMPC-grafted surface, and revealed considerable affinity to human umbilical vein endothelial cells (HUVEC), which is a well-known in vitro integrin α4β1-positive model. Better HUVEC spreading and proliferation was also confirmed, in terms of the cell extension property. Since coagulation and endothelialization on the materials compete in the body, they cannot be properly evaluated separately, in vitro. They were assessed by using an in situ porcine closed-circuit system for 18 h in the present study. Our findings suggest that poly(MPC-co-MAA) is a great ePTFE surface modifier, exhibiting good hemocompatibility in association with REDV/HCP-1 immobilization, which suppresses anti-platelet adhesion and enhances circulating cell capture simultaneously.
我们最近报道了通过聚(2-甲基丙烯酰氧乙基磷酸胆碱)(PMPC)表面接枝来抑制膨胀聚四氟乙烯(ePTFE)上血小板黏附的体外抑制作用。然而,这对于与血液接触的生物材料的长期血液相容性可能是不够的,这促使我们开发了一种循环单核细胞捕获策略。ePTFE 用氩(Ar)等离子体处理,并通过缩水甘油基甲基丙烯酸酯(GMA)锚定接枝聚合接枝 2-甲基丙烯酰氧乙基磷酸胆碱(MPC)和甲基丙烯酸(MAA)。接下来,它与整合素α4β1阳性循环血细胞特异性肽(即传统的精氨酸-谷氨酸-天冬氨酸-缬氨酸(REDV)和我们原始的血液相容性肽-1(HCP-1)固定。这两种表面都保留了与 PMPC 接枝表面相似的抗血小板特性,并显示出对人脐静脉内皮细胞(HUVEC)的相当大的亲和力,HUVEC 是一种众所周知的体外整合素α4β1阳性模型。从细胞延伸特性来看,还证实了更好的 HUVEC 扩展和增殖。由于在体内凝血和内皮化相互竞争,因此不能单独适当地进行体外评估。在本研究中,使用原位猪闭路系统评估了 18 小时。我们的研究结果表明,聚(MPC-co-MAA)是一种很好的 ePTFE 表面改性剂,与 REDV/HCP-1 固定相结合表现出良好的血液相容性,同时抑制抗血小板黏附和增强循环细胞捕获。