Immobilization of Glycogen Synthase Kinase-3β Inhibitor on 316L Stainless Steel via Polydopamine to Accelerate Endothelialization.

Ming Zhang,Donghua Xu,Yang Gao,Hai Sun,Jianqi Zhang,Xi Wu,Jichang Zhang,Xudong Shi

doi:10.3389/fbioe.2021.806151

Abstract

The coverage of stents with healthy endothelium is crucial to the success of cardiovascular stent implantation. Immobilizing bioactive molecules on stents is an effective strategy to generate such stents. Glycogen synthase kinase-3β inhibitor (GSKi) is a bioactive molecule that can effectively accelerate vascular endothelialization. In this work, GSKi was covalently conjugated on 316L stainless steel through polydopamine to develop a stable bioactive surface. Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM) and water contact angle results revealed the successful introduction of GSKi onto 316L stainless steel. The GSKi coating did not obviously affect the hemocompatibility of plates. The adhesion and proliferation of human coronary artery endothelial cells (HCAECs) on stainless steel was significantly promoted by the addition of GSKi. In summary, this work provides a universal and stable strategy of immobilizing GSKi on the stent surface. This method has the potential for widespread application in the modification of vascular stents.

Highlights

Coronary artery disease (CAD), especially myocardial infarction, is becoming a major cause of death worldwide and is responsible for more than 17.5 million deaths annually (Cui et al, 2018)
For the Glycogen synthase kinase-3β inhibitor (GSKi)-SS group, cell proliferation increased after incubation for 24 h and was further significantly enhanced after 48 h. These results showed that both polydopamine and GSKi coating on stainless steel plates can promote human coronary artery endothelial cells (HCAECs) proliferation
GSKi was successfully introduced on the surface of 316L stainless steel through polydopamine to form a stable bioactive coating

Summary

Introduction

Coronary artery disease (CAD), especially myocardial infarction, is becoming a major cause of death worldwide and is responsible for more than 17.5 million deaths annually (Cui et al, 2018). Drugeluting stents (DESs) have been successfully used in the treatment of CAD. Despite the success of DESs, a previous study demonstrated that in-stent restenosis (ISR) and late stent thrombosis (LST) represent obstacles to long-term application in the clinic (Otsuka et al, 2012; Liang et al, 2016). It was soon realized that the occurrences of ISR and LST are due to endothelial injury or the re-endothelialization delay of the stents (Kakinoki et al, 2018). A functionally intact vessel endothelium prevents thrombosis and mediates intimal hyperplasia. Reendothelialization on the stent effectively prevents ISR and LST (Woods and Marks, 2004). The selection of appropriate bioactive molecules and the strategy of immobilizing molecules on stents still need to be investigated

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Results

Conclusion