Endothelial nitric oxide synthase and fractalkine chemokine receptor polymorphisms on angiographically assessed coronary atherosclerosis

Rios, Domingos Lázaro Souza; Callegari-Jacques, Sídia M.; Hutz, Mara H.

doi:10.1016/j.cccn.2005.06.012

Cited by 26 publications

(16 citation statements)

References 41 publications

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“…Rios et al (2007) reported that smoking interacted with the À786C eNOS promoter variant increased the risk for CAD in Caucasian and African-Brazilian ethnic groups. In another study, significant association between À786 T=C polymorphism and severe CAD was found in the Brazilian population (Rios et al, 2005). A link between the CC genotype of this polymorphism and CAD has been found in independent studies including those in Chinese and Korean populations ( Jia et al, 2007;Kim et al, 2007).…”

Section: Discussionmentioning

confidence: 95%

“…Haplotype analysis has shown an association between the À786C=4-repeat=298E haplotype and the increased risk of CAD in Caucasian-Brazilian smokers (Rios et al, 2007). According to Rios et al (2005) there was an increased frequency of haplotypes carrying the À786C allele (À786C=298D and À786C=298E) in the CAD group. In our study, the distribution of the different haplotypes of eNOS in CADþ subjects was not different from that in CADÀ individuals ( p > 0.05).…”

Section: Discussionmentioning

confidence: 96%

“…According to a number of studies, G894T polymorphism (rs1799983) is associated with the occurrence and severity of myocardial infarction (MI), CAD, and stroke (Hibi et al, 1998;Hingorani et al, 1999;Colombo et al, 2002;Gardemann et al, 2002;McNamara et al, 2003). According to cross-sectional studies, the À786 T=C polymorphism (rs2070744), which reduces promoter activity, is highly associated with a blunted NO bioactivity in vivo (Rios et al, 2005;Rossi et al, 2006). This polymorphism has been associated with coronary spasm, MI, hypertension, and multivessel CAD in different populations (Nakayama et al, 1999Yoshimura et al, 2000;Hirashiki et al, 2003;Rossi et al, 2003aRossi et al, , 2003bCattaruzza et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Lack of Association Between Matrix Metalloproteinase-9 and Endothelial Nitric Oxide Synthase Gene Polymorphisms and Coronary Artery Disease in Turkish Population

Alp

Menevşe

Tulmaç³

et al. 2009

DNA and Cell Biology

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Polymorphic variants of genes encoding proteins involved in vascular remodeling may genetically diverge among different populations and play a role in the susceptibility to the coronary artery disease (CAD). MMP-9-1562 C/T (rs3918242), eNOS T-786C (rs2070744), and Glu298Asp (rs1799983) are among the most studied of these polymorphisms. The aim of this study was to determine the relationship between CAD and these polymorphisms in the Turkish population. The analysis included 146 CAD+ and 122 CAD- individuals. Genomic DNA was isolated from whole blood and genotyping was performed by the PCR-RFLP method. No significant associations were found between -1562 C/T (p = 0.557), Glu298Asp (p = 0.432), and -786 T/C (p = 0.055) polymorphisms and CAD. The distribution of each haplotype also did not differ between CAD+ and the CAD- samples (p > 0.05). The present investigation is the first to study an association between -1562 C/T polymorphism and CAD in the Turkish population. In conclusion, no appreciable differences between CAD+ and CAD- samples were found in terms of polymorphisms mentioned above.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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Lack of Association Between Matrix Metalloproteinase-9 and Endothelial Nitric Oxide Synthase Gene Polymorphisms and Coronary Artery Disease in Turkish Population

Alp

Menevşe

Tulmaç³

et al. 2009

DNA and Cell Biology

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“…The endothelial nitric oxide synthase (eNOS) gene presents some polymorphisms that have been previously associated with angiographically assessed CAD or myocardial infarct (MI) [3][4][5]. A functional variant in the eNOS promoter (T-786C) is associated with reduction in the promoter efficiency and the level of expressed enzyme leading to increased CAD risk [6][7][8]. The eNOS gene also presents a variable number of tandem repeats (27 bp) in intron 4, and the rare 4-repeat allele was associated with CAD [9].…”

Section: Introductionmentioning

confidence: 99%

Smoking-dependent and haplotype-specific effects of endothelial nitric oxide synthase gene polymorphisms on angiographically assessed coronary artery disease in Caucasian- and African-Brazilians

et al. 2007

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The nitric oxide produced by endothelial nitric oxide synthase (eNOS) plays a pivotal role in protecting the arterial wall from damages and atherosclerosis. The T-786C, the 27-bp repeat in intron 4, and the E298D eNOS gene polymorphisms were studied in 715 Brazilian patients (447 Caucasian- and 268 African-Brazilians) who underwent coronary angiography. The -786C frequency was increased in coronary artery disease (CAD) cases with significant lesions (> or =50% luminal obstruction) when compared with lesion-free controls; this difference was detected in smokers but not in nonsmokers, both in Caucasian- (p=0.011) and African-Brazilians (p=0.005). The interaction between -786C carriers and smoking was an independent CAD predictor (OR: 2.9, 95% CI: 1.4-5.9; p=0.003) in multiple logistic regression. The 298D mutation frequency was also higher among CAD cases (p=0.036) in African-Brazilian smokers, but this effect was not independent from other variables in the regression model. Though not associated with CAD, the 4-repeat allele combined with different T-786C alleles showed protective and susceptible effects in Caucasian-Brazilian smokers. The -786C/4-repeat/298E haplotype frequency was higher (p=0.020), whereas -786T/4-repeat/298E was lower (p=0.023) in these cases. These results showed a smoking-dependent effect of the T-786C eNOS polymorphism on CAD in both Caucasian- and African-Brazilians. Additionally, the haplotype analysis revealed different eNOS haplotypes associated with protection and susceptibility to the disease.

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“…In a sample from a southern Brazilian population of European ancestry studied by Rios et al (20), the ecNOS promoter -786T>C but not the ecNOS 894G>T polymorphism was associated with coronary artery disease (CAD) (20). Haplotype analysis showed that both haplotypes with a -786C allele (i.e., -766C/G and -786C/T) were predictors for CAD risk, suggesting, as did Tanus-Santos et al (21), that the promoter variant may be most relevant for the development of CAD in Caucasians.…”

Section: Introductionmentioning

confidence: 99%

Association of the 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene with unstable angina

Iturry-Yamamoto¹,

Moriguchi²,

Zago³

et al. 2007

Braz J Med Biol Res

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The 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene consists of the substitution of a guanine base by a thymine at the 894th nucleotide of the gene. An association of this polymorphism with acute coronary syndromes has been described, only when in combination with other polymorphisms of this gene. The aim of the present study was to search for an association between this polymorphism and unstable angina in a southern Brazilian population. In a case-control study, 156 patients (group 1 (N = 83): unstable angina, group 2 (N = 73): stable angina) were genotyped by PCR and digestion of the product. Univariate analysis demonstrated that the minimal luminal diameter and the degree of stenosis of the culprit lesion differed between groups (P = 0.006 and 0.005, respectively). In addition, the frequencies of the T allele and of the T allele carriers (combined TT and TG genotypes) were significantly higher in the group with unstable angina (41.6 vs 28.8%; P = 0.025, Pearson chisquare test, and 73.5 vs 45.2%; P = 0.001, Pearson chi-square test, respectively). Multivariate logistic regression showed that the frequency of the T allele carriers was the only variable with a predictive value for unstable angina, when controlled for the other variables (6.1 (95% CI = 2.55-14.43); P < 0.001). Thus, in a homogenous group of patients, the endothelial constitutive nitric oxide synthase 894G>T polymorphism was associated with unstable angina. We suggest that this polymorphism may be a genetic risk factor for unstable angina.

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Endothelial nitric oxide synthase and fractalkine chemokine receptor polymorphisms on angiographically assessed coronary atherosclerosis

Cited by 26 publications

References 41 publications

Lack of Association Between Matrix Metalloproteinase-9 and Endothelial Nitric Oxide Synthase Gene Polymorphisms and Coronary Artery Disease in Turkish Population

Lack of Association Between Matrix Metalloproteinase-9 and Endothelial Nitric Oxide Synthase Gene Polymorphisms and Coronary Artery Disease in Turkish Population

Smoking-dependent and haplotype-specific effects of endothelial nitric oxide synthase gene polymorphisms on angiographically assessed coronary artery disease in Caucasian- and African-Brazilians

Association of the 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene with unstable angina

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