Abstract
While drug-eluting stents containing anti-proliferative agents inhibit proliferation of smooth muscle cells (SMCs), they also delay the regrowth of the endothelial cells which can result in subsequent development of restenosis. Acidic extracellular environments promote cell anchorage and migration by inducing conformational change in integrins, the main cell adhesion proteins. This study addresses the feasibility of a citric acid (CA) functionalized nitinol stent for improving vascular biocompatibility, specifically enhancing endothelialization. CA functionalized nitinol vascular stents are compared to commercial bare metal (Zilver Flex) and paclitaxel eluting stents (Zilver PTX) in terms of re-endothelialization. To study the effect of stent coatings, a stent conditioned media methodology was developed in an attempt to represent in vivo conditions. Overall, distinct advantages of the CA functionalized nitinol stent over commercial Zilver PTX DES and Zilver Flex BMS stents in terms of endothelial cell adhesion, migration, and proliferation are reported. These novel findings indicate the potential of a CA functionalized stent to serve as a bioactive and therapeutic surface for re-endothelialization, perhaps in combination with a SMC proliferation inhibitor coating, to prevent restenosis.
Highlights
Endothelial denudation followed by an impaired or incomplete healing of the intimal layer has been a major problem associated with vascular stent implantation for decades
It is recognized that accelerated endothelialization can prevent neointimal proliferation, which results in the thickening of vascular wall and restenosis
mouse cardiac endothelial (MCE) cell migration demonstrates that an extracellular acidic environment, as in the case of the citric acid functionalised stent (CAFS) conditioned media, significantly enhances cell migration at 2 hr in vitro
Summary
Endothelial denudation followed by an impaired or incomplete healing of the intimal layer has been a major problem associated with vascular stent implantation for decades. The use of DES brings with it a new issue of late stent thrombosis associated with a disruption of the cells' post-injury healing mechanism.[2,3] The process of migration and proliferation of EC has been shown to be impaired by the action of the anti-proliferative agent, paclitaxel, which suppresses smooth muscle cell (SMC) proliferation and endothelial cell proliferation, potentially affecting the reendothelialization process.[3,4,5] Human studies suggest the time required for complete endothelialization after BMS implantation is between 3 and 4 months,[6] while re-endothelialization after DES implantation has been shown to be significantly delayed, in some cases beyond 12 months.[3]
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