A nitric oxide-generating polymeric coating was prepared
by copolymerization
of the hydrophilic monomer 2-hydroxyethyl methacrylate (HEMA) and
the comonomer 1-adamantan-1-ylmethyl methacrylate (AdaMA) with subsequent
incorporation of selenocystamine. The coating was applied to polyurethane
(PU) as a substrate. In the presence of a NO donor, the PU–PHA-Se
surface generated nitric oxide (NO). This surface was shown to inhibit
platelet adhesion and human umbilical vein smooth muscle cell adhesion
and proliferation. The poly(AdaMA) on the modified surface was designed
to allow the incorporation of functional units into the PU–PHA-Se
surface via host–guest interactions between the adamantane
groups and cyclodextrin (CD) derivatives. In this work, two functional
CD complexes containing lysine (CD-L) and sulfonate (CD-S) groups
were incorporated into the PU–PHA-Se surface. CD-L conferred
fibrinolytic activity, whereas CD-S promoted human umbilical vein
endothelial cell proliferation. This NO-generating antiplatelet polymeric
coating has potential as a platform for modifying surfaces with multiple
additional biological functions via host–guest interactions,
thus providing an alternative approach for the preparation of biomaterials
with multifunctionality.
Heparin-like polymers are promising synthetic materials with similar biological functionalities as heparin, such as anticoagulant ability, growth factor binding to regulate cellular functions, and inflammation mediation. The biocompatibility of heparin-like...
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