TY - JOUR
T1 - Endothelial nitric oxide synthase gene is associated with vessel stenosis in Korean population
AU - Yoon, Suin
AU - Shin, Chol
AU - Park, Hyun Young
AU - Moon, Jesung
AU - Kim, Eunkyung
AU - Kim, Heung Tae
AU - Min, Jiho
AU - Jo, Sangmee Ahn
AU - Jo, Inho
N1 - Funding Information:
This work was supported in part by research grant from Ministry of Health and Welfare (HMP-00-P-21900-0017) to Drs. Inho Jo, Chol Shin and Hyun-Young Park. We thank Dr. Ho Kim for statistical analysis, Dr. Jin-Sung Lee for DNA preparation and invaluable suggestions and Ms. Jooyoung Lee and Ms. Sun Mi Lee for secretarial assistance.
PY - 2005/3
Y1 - 2005/3
N2 - Background: Nitric oxide (NO) produced by endothelial NO synthase (eNOS) mediates endothelium-dependent vasodilation and antithrombotic action. Controversial results regarding the association of eNOS gene polymorphisms with vessel stenosis have been reported. Methods: Age- and sex-matched 932 individuals (656 subjects having 1-, 2-, and 3-stenosed vessels and 276 controls without stenosis) living in Seoul and surrounding suburbs were selected. A GT missense mutation in exon 7 (894GT) was screened using PCR-restriction fragment length polymorphism analysis. The genotypes of a 27-bp insertion/deletion in intron 4 (eNOS4b/a) and a TC mutation in promoter region of -786 (-786TC) were determined by the banding pattern on gel electrophoresis and a commercially available minisequencing protocol (SNaPshot), respectively. Results: The eNOS4a allele was highly linked to the -786C allele (r=0.93, P<0.0001) while there was no linkage between eNOS4a allele and 894T allele or between 894T allele and -786C allele. Furthermore, 894T allele, but not eNOS4a (-786C) allele, was associated with the presence, but not the number, of stenosed vessels (odds ratio=1.57 for dominant effect of the T allele, P<0.05, and 1.49 for additive effect, P<0.05). Multiple logistic regression analysis revealed that 894T allele and hypertension were predictive independent risk factors for the presence of vessel stenosis. Conclusion: Our data suggest that eNOS gene polymorphisms may play an important role in the pathogenesis of vessel stenosis in Korean population.
AB - Background: Nitric oxide (NO) produced by endothelial NO synthase (eNOS) mediates endothelium-dependent vasodilation and antithrombotic action. Controversial results regarding the association of eNOS gene polymorphisms with vessel stenosis have been reported. Methods: Age- and sex-matched 932 individuals (656 subjects having 1-, 2-, and 3-stenosed vessels and 276 controls without stenosis) living in Seoul and surrounding suburbs were selected. A GT missense mutation in exon 7 (894GT) was screened using PCR-restriction fragment length polymorphism analysis. The genotypes of a 27-bp insertion/deletion in intron 4 (eNOS4b/a) and a TC mutation in promoter region of -786 (-786TC) were determined by the banding pattern on gel electrophoresis and a commercially available minisequencing protocol (SNaPshot), respectively. Results: The eNOS4a allele was highly linked to the -786C allele (r=0.93, P<0.0001) while there was no linkage between eNOS4a allele and 894T allele or between 894T allele and -786C allele. Furthermore, 894T allele, but not eNOS4a (-786C) allele, was associated with the presence, but not the number, of stenosed vessels (odds ratio=1.57 for dominant effect of the T allele, P<0.05, and 1.49 for additive effect, P<0.05). Multiple logistic regression analysis revealed that 894T allele and hypertension were predictive independent risk factors for the presence of vessel stenosis. Conclusion: Our data suggest that eNOS gene polymorphisms may play an important role in the pathogenesis of vessel stenosis in Korean population.
KW - Endothelial nitric oxide synthase gene
KW - Korea
KW - Polymorphism
KW - Vessel stenosis
UR - http://www.scopus.com/inward/record.url?scp=13444256171&partnerID=8YFLogxK
U2 - 10.1016/j.cccn.2004.10.018
DO - 10.1016/j.cccn.2004.10.018
M3 - Article
C2 - 15698605
AN - SCOPUS:13444256171
SN - 0009-8981
VL - 353
SP - 177
EP - 185
JO - Clinica Chimica Acta
JF - Clinica Chimica Acta
IS - 1-2
ER -