Association study of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with myocardial infarction

Iqbal, Mohammad Perwaiz; Saeed, Mohammad; Mehboobali, Naseema; Ishaq, Mohammad; Fatima, Tasnim; Parveen, Saddiqa; Frossard, Philippe

doi:10.1038/emm.2004.16

Cited by 11 publications

(5 citation statements)

References 26 publications

(22 reference statements)

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“…A allele carrier is an independent risk factor for acute MI after adjustments for age, gender, BMI, smoking status, blood pressure, and plasma levels of lipids and apolipoproteins. This result was not in agreement with the only reported study carried out in the Emirati population, 29 which showed no significant difference in distribution of the 3 genotypes between MI patients and controls (χ 2 = 3.1, P = .217). However, in their study, the ACE2350G>A genotypes were not in agreement with predicted Hardy-Weinberg equilibrium values, either in the normal control group or in acute MI patients.…”

Section: Discussioncontrasting

confidence: 95%

Association of Angiotensin-Converting Enzyme Gene 2350G>A Polymorphism With Myocardial Infarction in a Chinese Population

Pan

Jiang

Wei

et al. 2008

Clin Appl Thromb Hemost

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Angiotensin-converting enzyme (ACE) gene 2350G>A polymorphism has the most significant effect on plasma ACE concentrations. But the association between this polymorphism and myocardial infarction (MI) is presently unknown. We carried out a case-control study in the Chinese Han population. ACE2350G>A genotypes of 231 patients with MI and 288 healthy controls were detected by PCR-RFLP. Differences in frequencies of ACE genotypes and alleles and their associations with clinical features were assessed. The distribution of the ACE2350G>A genotypes (GG, GA, and AA) was 20.78%, 51.08%, and 28.14% in the MI group and 31.60%, 46.53%, and 21.87% in controls, respectively (P = .0167).The frequency of the A allele in the MI group was significantly higher than that in controls (53.68% vs 45.14%, P = .0062). The A allele carriers (GA + AA genotypes) had approximately 2-fold increased risk of MI when compared with the GG genotype (odds ratio = 1.76; 95% confidence interval = 1.24-3.52). There were no significant differences among the 3 genotypes in plasma levels of lipids, apolipoproteins, high-sensitivity C-reactive protein, and soluble CD40 ligand in either the MI group or the control group (P > .05). No statistical difference was observed between ACE2350G>A polymorphism and severity of the coronary lesions (P > .05). These results suggest that ACE2350G>A polymorphism is associated with acute MI, and A allele carrier is an independent risk factor for acute MI in the Chinese Han population.

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Section: Discussioncontrasting

confidence: 95%

Association of Angiotensin-Converting Enzyme Gene 2350G>A Polymorphism With Myocardial Infarction in a Chinese Population

Pan

Jiang

Wei

et al. 2008

Clin Appl Thromb Hemost

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“…Several investigators found no association with the occurrence of either CAD, MI 46–50 or long-term clinical outcomes, 51 while others demonstrated a positive association between especially the D allele and ischemic heart disease generally or for certain subgroups of patients. 31,37,46,48–50,52–54 Assessing six different genetic polymorphisms of the RAS components in a group of CAD patients was based on the study hypothesis that the influence of genetic polymorphisms on the activity of ACE or Ang II receptors could show measurable effects on CRP plasma levels in atherosclerosis. This could even provide clues relating ACE I/D genetic polymorphism to the inflammatory component of atherosclerosis in patients with CAD.…”

Section: Discussionmentioning

confidence: 99%

“…35 PCR amplification of A-240T, A2350G, M235T, A1166C, and C3123A was performed using primers mentioned in Table 1. 25,34,36–40 In each reaction, 100–200 ng of genomic DNA was amplified in 15 µl of 1×PCR master mix (67 mM Tris base, pH 8.8, 16.6 mM (NH4) 2SO4, 2 mM MgCl2, 0.1% Tween-20, 200 µM deoxyribonucleotide triphosphates (dNTPs), 5% glycerol, 100 µg/ml cresol red) containing 0.2–2.0 µM of each primer and 0.5 U of Taq DNA polymerase (Cinnagen Inc, Tehran, Iran). All genes were amplified under the same procedure, which is of great advantage to reduce workload.…”

Section: Methodsmentioning

confidence: 99%

Renin–angiotensin system genetic polymorphisms: Lack of association with CRP levels in patients with coronary artery disease

Bahramali

Firouzabadi

Jonaidi-Jafari

et al. 2013

J Renin Angiotensin Aldosterone Syst

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Angiotensin (Ang) II is believed to be a potential pro-inflammatory factor. The capability of Ang II to stimulate C-reactive protein (CRP) production has recently been described. Genetic polymorphisms of renin angiotensin system (RAS) components have been described to be associated with the development of coronary artery disease (CAD). This study investigated the association between six different genetic polymorphisms of RAS and serum CRP levels in a sample of CAD patients. Genotyping of RAS genes polymorphisms in 176 patients with documented CAD was performed by a modified polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Measurement of high-sensitivity (hs)-CRP was performed using standard immunoturbidimetric methods. Results show no significant differences in serum CRP regarding different variants of the six polymorphisms studied (p = 0.41, 0.24, 0.25, 0.19, 0.29, and 0.05 for Ang-converting enzyme (ACE) insertion/deletion (I/D), A-240T and A2350G, angiotensinogen M235T, AT1 receptor A1166C, and AT2 receptor C3123A polymorphisms, respectively). In conclusion, genetic polymorphisms of RAS are not associated with increased serum CRP in CAD. Compensation of an increased activity of ACE through counter-regulation and the secretion of CRP under the influence of Ang II in the vessel being local could explain the lack of association between the studied polymorphisms and CRP levels in CAD patients.

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“…The extracted DNAs were stored at -20 °C for polymerase chain reaction restriction fragment length polymorphism (PCR–RFLP) analysis. PCR amplification of G8790A and A2350G was performed using primers mentioned in Table 2 [ 51 , 52 ]. PCR amplification/detection of G8790A was performed as described previously [ 53 ].…”

Section: Methodsmentioning

confidence: 99%

SNPs of ACE1 (rs4343) and ACE2 (rs2285666) genes are linked to SARS-CoV-2 infection but not with the severity of disease

Alimoradi

Sharqi

Firouzabadi

et al. 2022

Virol J

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COVID-19 and the renin-angiotensin system (RAS) are linked by angiotensin-converting enzyme 2 (ACE2), a key enzyme in RAS that has been validated as a SARS-CoV-2 receptor. Functional ACE1/ACE2 gene polymorphisms may lead to the imbalance between ACE/ACE2 ratio and thus generating RAS imbalance that is associated with higher degrees of lung damage in ARDS that may contribute to the COVID-19 infection outcome. Herein, we investigated the role of RAS gene polymorphisms, ACE1 (A2350G) and ACE2 (G8790A) as risk predictors for susceptibility and severity of COVID-19 infection. A total of 129 included: negative controls without a history of COVID-19 infection (n = 50), positive controls with a history of COVID-19 infection who were not hospitalized (n = 35), and patients with severe COVID-19 infection who were hospitalized in the intensive care unit (n = 44). rs4343 of ACE and rs2285666 of ACE2 were genotyped using PCR–RFLP method. Our results indicated that susceptibility to COVID-19 infection was associated with age, GG genotype of A2350G (Pa = 0.01; OR 4.7; 95% CI 1.4–15.1 and Pc = 0.040; OR 2.5; 95% CI 1.05–6.3) and GG genotype of G8790A (Pa = 0.044; OR 6.17; 95% CI 1.05–35.71 and Pc = 0.0001; OR 5.5; 95% CI 2.4–12.4). The G allele of A2350G (Pa = 0.21; OR 1.74; 95% CI 0.73–4.17 and Pc = 0.007; OR 2.1; 95% CI 1.2–3.5) and G allele of G8790A (Pa = 0.002; OR 4.26; 95% CI 1.7–10.65 and Pc = 0.0001; OR 4.7; 95% CI 2.4–9.2) were more frequent in ICU-admitted patients and positive control group. Also lung involvement due to COVID-19 infection was associated with age and the comorbidities such as diabetes. In conclusion, our findings support the association between the wild genotype (GG) of ACE2 and homozygote genotype (GG) of ACE1 and sensitivity to COVID-19 infection, but not its severity. However, confirmation of this hypothesis requires further studies with more participants.

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Association study of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with myocardial infarction

Cited by 11 publications

References 26 publications

Association of Angiotensin-Converting Enzyme Gene 2350G>A Polymorphism With Myocardial Infarction in a Chinese Population

Association of Angiotensin-Converting Enzyme Gene 2350G>A Polymorphism With Myocardial Infarction in a Chinese Population

Renin–angiotensin system genetic polymorphisms: Lack of association with CRP levels in patients with coronary artery disease

SNPs of ACE1 (rs4343) and ACE2 (rs2285666) genes are linked to SARS-CoV-2 infection but not with the severity of disease

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