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논문번호 27
논문제목(영문) The effects of granulocyte-colony stimulating factor in bare stent and sirolimus-eluting stent in pigs following myocardial infarction.
국내외구분 국외 SCI여부 SCI(E)
연구책임자역할 공저자
주저자명 Lim SY, Kim YS
교신저자명 Ahn Y
공동저자명 Lim SY, Kim YS, Ahn Y, Jeong MH, Rok LS, Kim JH, Kim KH, Park HW, Kim W, Cho JG, Park JC, Kang PM, Schwartz RS, Kang JC;
게제년월일 2006-07-09
ISSN 0167-5273
Impact Factor 4.063
학술지명 International journal of cardiology
서지사항 0집 / 118권 / 3호,   페이지(304 - 311)
요약초록문
(Abstract) 입력		 OBJECTIVES:
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.
BACKGROUND:
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.
METHODS:
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, n=10 in each group) 72 h after experimental myocardial infarction (MI). G-CSF (10 microg/kg/day) was injected for 7 days from 24 h after stent implantation.
RESULTS:
In coronary angiographic and histomorphometric analysis, percent area stenosis was significantly increased in Group II compared with that in Group I at 28 days (P<0.05). The ratio of inflammatory cells in the neointima was higher in Group II (P<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.
CONCLUSIONS:
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.
파일  B27. Int J Cardiol. 2007;118(3)304-311..pdf (761.0K) DATE : 2016-03-13 08:05:18