Abstract
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 μg/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.
| Original language | English |
|---|---|
| Pages (from-to) | 304-311 |
| Number of pages | 8 |
| Journal | International Journal of Cardiology |
| Volume | 118 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2007 Jun 12 |
| Externally published | Yes |
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Keywords
- Bare stent
- Granulocyte-colony stimulating factor
- In-stent restenosis
- Sirolimus-eluting stent
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
The effects of granulocyte-colony stimulating factor in bare stent and sirolimus-eluting stent in pigs following myocardial infarction. / Lim, Sang Yeob; Kim, Yong Sook; Ahn, Youngkeun; Jeong, Myung Ho; Rok, Lee Sang; Kim, Ju Han; Kim, Key Hun; Park, Hyung Wook; Kim, Weon; Cho, Jeong Gwan; Park, Jong Chun; Kang, Peter M.; Schwartz, Robert S.; Kang, Jung Chaee.
In: International Journal of Cardiology, Vol. 118, No. 3, 12.06.2007, p. 304-311.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The effects of granulocyte-colony stimulating factor in bare stent and sirolimus-eluting stent in pigs following myocardial infarction
AU - Lim, Sang Yeob
AU - Kim, Yong Sook
AU - Ahn, Youngkeun
AU - Jeong, Myung Ho
AU - Rok, Lee Sang
AU - Kim, Ju Han
AU - Kim, Key Hun
AU - Park, Hyung Wook
AU - Kim, Weon
AU - Cho, Jeong Gwan
AU - Park, Jong Chun
AU - Kang, Peter M.
AU - Schwartz, Robert S.
AU - Kang, Jung Chaee
PY - 2007/6/12
Y1 - 2007/6/12
N2 - 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 μg/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.
AB - 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 μg/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.
KW - Bare stent
KW - Granulocyte-colony stimulating factor
KW - In-stent restenosis
KW - Sirolimus-eluting stent
UR - http://www.scopus.com/inward/record.url?scp=34247601112&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34247601112&partnerID=8YFLogxK
U2 - 10.1016/j.ijcard.2006.07.018
DO - 10.1016/j.ijcard.2006.07.018
M3 - Article
C2 - 17052793
AN - SCOPUS:34247601112
VL - 118
SP - 304
EP - 311
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
IS - 3
ER -