No abstract

Drug-eluting stents (DES) have been widely used to treat coronary artery disease (CAD) since their clinical use has significantly reduced the occurrence of in-stent restenosis (ISR) as compared with the initially applied bare-metal stents (BMS). However, analyses of long-term clinical outcome have raised concerns about the serious safety problem of DES, such as ISR caused by late or very late thrombosis. Various studies showed that those complications were associated with vascular endothelial injury/dysfunction or endothelialization delaying. Recently, through biological characterization of endothelial progenitor cells (EPCs), mechanistic understanding of rapid re-endothelialization of the vascular injury sites after coronary stenting has become possible and is a new research hotspot in the prevention of ISR and late/very late stent thrombosis. It has been well recognized that the formation of a functional endothelial layer from EPCs requires a coordinated sequence of multistep and signaling events, which includes cell mobilization, adhesion, migration and finally the differentiation to vascular endothelial cells (VECs). In this review, we summarize and discuss the currently relevant information about EPCs, the mechanism of DES interfering with the natural vascular healing process in preventing or delaying the formation of a functional endothelial layer, and EPCs-mediated acceleration of re-endothelialization at vascular injury sites. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1237-1247, 2016.

It is widely accepted that surface biofunctional modification may be an effective approach to improve biocompatibility and confer new bioactive properties on biomaterials. In this work, mussel adhesive protein (MAP) was applied as a coating on 316L stainless steel substrates (316L SS) and stents, and then either immobilized VEGF or CD34 antibody were added to create biofunctional films. The properties of the MAP coating were characterized by scanning electron microscope (SEM), atomic force microscope (AFM) and water contact angle test. Universal tensile testing showed that the MAP coating has adequate adhesion strength on a 316L stainless steel material surface. Subsequent cytotoxicity and hemolysis rate tests showed that the MAP coatings have good biocompatibility. Moreover, using N-(3-Dimethylaminopropyl)-N`-ethylcarbodiimide hydrochloride and Nhydroxysulfosussinimide (EDC/NHS) chemistry, VEGF and CD34 antibody were immobilized on the MAP coatings. The amount and immobilized yield of VEGF on the MAP coatings were analyzed by enzyme-linked immuno-assays (ELISA). Finally, an endothelial cells culture showed that the VEGF biofunctional film can promote the viability and proliferation of endothelial cells. An in vitro CD34 + cells capturing test also verified the bioactive properties of the CD34 antibody coated stents. These results showed that the MAP coatings allowed effective biomolecule immobilization, providing a promising platform for vascular device modification.