title: The effects of granulocyte-colony stimulating factor in bare stent and sirolimus-eluting stent in pigs following myocardial infarction.
abstract: OBJECTIVE
  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.
authors.affiliation: The Heart Center of Chonnam National University Hospital, Gwangju, South Korea.
authors.forename: Sang Yup
authors.initials: SY
authors.lastname: Lim
authors.forename: Yong Sook
authors.initials: YS
authors.lastname: Kim
authors.forename: Youngkeun
authors.initials: Y
authors.lastname: Ahn
authors.forename: Myung Ho
authors.initials: MH
authors.lastname: Jeong
authors.forename: Lee Sang
authors.initials: LS
authors.lastname: Rok
authors.forename: Ju Han
authors.initials: JH
authors.lastname: Kim
authors.forename: Key Hun
authors.initials: KH
authors.lastname: Kim
authors.forename: Hyung Wook
authors.initials: HW
authors.lastname: Park
authors.forename: Weon
authors.initials: W
authors.lastname: Kim
authors.forename: Jeong Gwan
authors.initials: JG
authors.lastname: Cho
authors.forename: Jong Chun
authors.initials: JC
authors.lastname: Park
authors.forename: Peter M
authors.initials: PM
authors.lastname: Kang
authors.forename: Robert S
authors.initials: RS
authors.lastname: Schwartz
authors.forename: Jung Chaee
authors.initials: JC
authors.lastname: Kang
mesh_terms: D000704:Analysis of Variance; D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D001774:Blood Chemical Analysis; D049109:Cell Proliferation / Q000187:drug effects; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D007150:Immunohistochemistry; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000628:therapy*; D011336:Probability; D011897:Random Allocation; D012680:Sensitivity and Specificity; D020123:Sirolimus / Q000494:pharmacology*; D015607:Stents; D034421:Sus scrofa
chemical_list: D016179:Granulocyte Colony-Stimulating Factor; D020123:Sirolimus