Aims: Although the use of drug-eluting stents (DES) has been shown to limit neointimal hyperplasia in clinical coronary artery disease treatment, currently available DES may adversely affect re-endothelialization (RE) and thus increase fateful stent thrombosis. As stromal cell derived factor 1a (SDF-1a) plays an essential role in the regulation of endothelial progenitor cells (EPCs) mobilization, homing, and differentiation in response to vascular injury, we assumed that SDF-1a may enhance EPCs adhesion and attenuate delayed RE associated with DES.
Main methods: Biologically active recombinant human SDF-1a (rhSDF-1a) was first produced using an Escherichia coli expression system. Twenty-four male rabbits were then underwent sirolimus-eluting stents implantation in aorta abdominalis. After operation, they were randomly divided into two groups and subcutaneously injected daily with 50 μg/kg rhSDF-1a or the same volume of saline for 7 days.
Key findings: With the application of scanning electron microscopy (SEM) and histological analysis, we found that rhSDF-1a significantly promoted RE on days 7, 14, 28 and inhibited neointimal hyperplasia on day 28 after stent implantation.
Significance: Our results revealed a potential role of rhSDF-1a in facilitating RE and inhibiting neointimal proliferation after DES implantation, leading to a conclusion that this protein may be a potential candidate agent for the treatment of in-stent restenosis and stent thrombosis.
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