TY - JOUR
T1 - Association of RAGE gene polymorphisms with in-stent restenosis in non-diabetic Korean population
AU - Shim, Chi Young
AU - Park, Sungha
AU - Yoon, Se Jung
AU - Park, Hyun Young
AU - Kim, Hung Tae
AU - Oh, Bermseok
AU - Park, Chanmi
AU - Ko, Young Guk
AU - Choi, Donghoon
AU - Jang, Yangsoo
AU - Chung, Namsik
PY - 2007/5
Y1 - 2007/5
N2 - Backgrounds: Interaction between advanced glycosylation end products (AGEs) and receptor for AGEs (RAGE) in vessel wall may lead to inflammation, smooth muscle cell proliferation, and extracellular matrix production, culminating in exaggerated intimal hyperplasia and restenosis. We investigated the possibility that single nucleotide polymorphisms of the genes encoding RAGE are associated with in-stent restenosis after coronary stenting. Methods: Our study included 334 consecutive non-diabetic male patients with symptomatic coronary artery disease who underwent bare metal stent implantation. Follow-up angiography was performed in 297 patients (88.9%), 6 months after intervention. We screened -1106T→C, -443T→C, -388T→A, -257G→A, +557G→A and +1704G→T RAGE polymorphisms in these patients. Genotyping was performed by single base extension with amplifying primers and probes for TaqMan. Results: A total of 355 target lesions were evaluated, in 297 patients. There was no significant association of the -1106T→C, -443T→C, -388T→A, -257G→A, +557G→A or +1704G→T polymorphisms with in-stent restenosis after coronary artery stenting. We did not observe a significant difference between the genotype distributions and the rates of angiographic restenosis between the polymorphisms. In a multivariate analysis of angiographic restenosis, we examined the possible influence of the baseline, lesion-related, and procedural variables. After adjustment for these potentially confounding factors, the multivariate analysis did not reveal an association of polymorphism with angiographic restenosis. Conclusion: Our observation suggests that the RAGE gene polymorphism is not associated with in-stent restenosis after coronary artery stenting in non-diabetic patients in the Korean population.
AB - Backgrounds: Interaction between advanced glycosylation end products (AGEs) and receptor for AGEs (RAGE) in vessel wall may lead to inflammation, smooth muscle cell proliferation, and extracellular matrix production, culminating in exaggerated intimal hyperplasia and restenosis. We investigated the possibility that single nucleotide polymorphisms of the genes encoding RAGE are associated with in-stent restenosis after coronary stenting. Methods: Our study included 334 consecutive non-diabetic male patients with symptomatic coronary artery disease who underwent bare metal stent implantation. Follow-up angiography was performed in 297 patients (88.9%), 6 months after intervention. We screened -1106T→C, -443T→C, -388T→A, -257G→A, +557G→A and +1704G→T RAGE polymorphisms in these patients. Genotyping was performed by single base extension with amplifying primers and probes for TaqMan. Results: A total of 355 target lesions were evaluated, in 297 patients. There was no significant association of the -1106T→C, -443T→C, -388T→A, -257G→A, +557G→A or +1704G→T polymorphisms with in-stent restenosis after coronary artery stenting. We did not observe a significant difference between the genotype distributions and the rates of angiographic restenosis between the polymorphisms. In a multivariate analysis of angiographic restenosis, we examined the possible influence of the baseline, lesion-related, and procedural variables. After adjustment for these potentially confounding factors, the multivariate analysis did not reveal an association of polymorphism with angiographic restenosis. Conclusion: Our observation suggests that the RAGE gene polymorphism is not associated with in-stent restenosis after coronary artery stenting in non-diabetic patients in the Korean population.
KW - Coronary artery disease
KW - In-stent restenosis
KW - Receptor for advanced glycation end products
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U2 - 10.1159/000095516
DO - 10.1159/000095516
M3 - Article
C2 - 16954682
AN - SCOPUS:34249042954
SN - 0008-6312
VL - 107
SP - 261
EP - 268
JO - Cardiology
JF - Cardiology
IS - 4
ER -