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• W2068203418 abstract "<h2>Abstract</h2><h3>Objectives</h3> The purpose of this study was to compare the effects of granulocyte-colony stimulating factor (G-CSF) on in-stent restenosis (ISR) in bare and sirolimus-eluting stents (SES) in a porcine myocardial infarction model. <h3>Background</h3> Using G-CSF to mobilize stem cells has shown promise in infarcted heart. However, G-CSF may aggravate ISR and an aggressive strategy to prevent ISR is needed. <h3>Methods</h3> Bare stents and SES were implanted in coronary arteries (Group I, bare stents; Group II, bare stents with G-CSF; Group III, SES; Group IV, SES with G-CSF, <i>n</i>=10 in each group) 72 h after experimental myocardial infarction (MI). G-CSF (10 μg/kg/day) was injected for 7 days from 24 h after stent implantation. <h3>Results</h3> In coronary angiographic and histomorphometric analysis, percent area stenosis was significantly increased in Group II compared with that in Group I at 28 days (<i>P</i><0.05). The ratio of inflammatory cells in the neointima was higher in Group II (<i>P</i><0.05). No significant differences were observed between Group III and IV. In Group II, phosphorylated signal transducers and activators of transcription (STAT)-3, STAT-3, and vascular endothelial growth factor (VEGF) showed increased neointimal expression. In porcine aortic smooth muscle cells (PASMC), G-CSF increased the growth rate, migration, STAT-3 phosphorylation, and VEGF, which were suppressed by rapamycin and AG490, a STAT-3 inhibitor. <h3>Conclusions</h3> STAT-3 and VEGF are important in the development of enhanced ISR by G-CSF in bare stents. SES could be a good strategy to prevent the G-CSF-stimulated proliferation and migration of smooth muscle cells, which could be responsible for neointimal hyperplasia." @default.
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• W2068203418 date "2007-06-01" @default.
• W2068203418 modified "2023-10-16" @default.
• W2068203418 title "The effects of granulocyte-colony stimulating factor in bare stent and sirolimus-eluting stent in pigs following myocardial infarction" @default.
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• W2068203418 doi "https://doi.org/10.1016/j.ijcard.2006.07.018" @default.
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