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. 2017 Dec;26(4):218-222.
doi: 10.1055/s-0037-1601871. Epub 2017 Apr 16.

Vitronectin and Urokinase-Type Plasminogen Activator Gene Expression Levels Are Increased in Patients with Coronary Artery In-Stent Restenosis

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Vitronectin and Urokinase-Type Plasminogen Activator Gene Expression Levels Are Increased in Patients with Coronary Artery In-Stent Restenosis

S M Shafiee et al. Int J Angiol. 2017 Dec.

Abstract

Neointimal hyperplasia is known as a main factor contributing to in-stent restenosis (ISR). Monocytes may play a central role in vessel restenosis process after stent implantation. The aim of this study was to investigate the relationships between the urokinase-type plasminogen activator (PLAU) and vitronectin (Vtn) gene expression levels in peripheral blood mononuclear cell samples isolated from whole blood of 66 patients undergoing coronary artery angiography (22 controls, stenosis < 0.05%; 22 with stent no-restenosis and stenosis < 70%; and 22 with ISR and stenosis > 70%). The Vtn and PLAU gene expression levels were measured by real-time quantitative polymerase chain reaction technique. The age- and gender-independent increases in the expression levels of Vtn (17-fold; p < 0.001) and PLAU (27-fold; p < 0.0001) genes were found in the patients with ISR as compared with the control group. The results suggested that the Vtn and PLAU genes may be involved in the coronary artery ISR.

Keywords: in-stent restenosis; urokinase-type plasminogen activator; vitronectin.

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Figures

Fig. 1
Fig. 1
Urokinase-type plasminogen activator gene expression levels in study groups. Control (stenosis < 5%), stent no-restenosis (SNR) < 70%, and in-stent restenosis (ISR) >70%. ISR versus control and SNR; p  < 0.0001.
Fig. 2
Fig. 2
Vitronectin gene expression levels in study groups. Control (stenosis < 5%), stent no-restenosis (SNR) <70%, in-stent restenosis (ISR) >70%. ISR versus control and SNR; p  < 0.001.

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References

    1. Yang Z K, Shen Y, Hu J et al.Impact of coronary collateral circulation on angiographic in-stent restenosis in patients with stable coronary artery disease and chronic total occlusion. Int J Cardiol. 2017;227:485–489. - PubMed
    1. Fischman D L, Leon M B, Baim D S et al.A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med. 1994;331(08):496–501. - PubMed
    1. Indolfi C, Pavia M, Angelillo I F. Drug-eluting stents versus bare metal stents in percutaneous coronary interventions (a meta-analysis) Am J Cardiol. 2005;95(10):1146–1152. - PubMed
    1. Denes L, Entz L, Jancsik V. Restenosis and therapy. Int J Vasc Med. 2012;2012:406236. - PMC - PubMed
    1. Serruys P W, de Jaegere P, Kiemeneij F et al.A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med. 1994;331(08):489–495. - PubMed