Plasma treatment of polymer surfaces can modify the nanoscale roughness, wettability, and oxygen surface functionalities. However, how these modifications regulate cell behavior is not well understood. The objective of this investigation was to examine adhesion, spreading, and cytoskeleton of vascular endothelial cells seeded on low-density polyethylene surfaces modified by Ar plasma. In the absence of serum, adhesion and spreading of the cells and actin filament assembly were enhanced by high-energy Ar plasma-induced hydrophilicity and formation of C-O groups at the surface. Although serum increased cell adhesion and spreading on untreated surfaces for a relatively short period, this behavior was not stable for a long time. In contrast to the untreated polymer surfaces, serum suppressed cell adhesion and spreading on the plasma-treated surfaces. The preadsorption of albumin from the bovine serum on the polymer surfaces inhibited cell adhesion and spreading. Results demonstrate the differential effects of Ar plasma-induced surface modifications on endothelial cell behavior and provide insight into complex interactions among polymer surfaces, adsorbed proteins, and cells. The findings of this study have significant implications in surface engineering for vascular repair.

No abstract

Heparin conjugation of poly(L-lactide) fibrous scaffolds fabricated by electrospinning was accomplished by surface functionalization with amine (–NH2) groups using a sequential treatment with Ar-NH3 and H2 plasmas. The density of the incorporated –NH2 group was determined by combining a chemical derivatization method with X-ray photoelectron spectroscopy. The time of Ar-NH3 plasma treatment significantly affected the N/C, –NH2/N, and –NH2/C fractions, whereas the plasma power, Ar-NH3 gas composition, and time of H2 plasma treatment only influenced the –NH2/N and –NH2/C fractions. Scaffold surface functionalization by –NH2 groups significantly increased the amount of covalently bonded heparin compared to a hydrolysis method. The function of immobilized heparin was confirmed by the decrease of platelet attachment during the exposure of the scaffolds to blood from Sprague-Dawley rats. In vitro experiments with bovine aorta endothelial cells demonstrated that heparin conjugation enhanced cell infiltration through the fibrous scaffolds, regardless of the amount of covalently immobilized heparin.