Association between the −2518G/A polymorphism in the monocyte chemoattractant protein-1 (MCP-1) gene and myocardial infarction in Tunisian patients

Jemaa, Riadh; Rojbani, Hajer; Kallel, Amani; Ali, Samir Ben; Feki, Moncef; Chabrak, Sonia; Elasmi, Monia; Taieb, Samah Haj; Sanhaji, Haïfa; Omar, Souheil; Mechmèche, Rachid; Kaabachi, Naziha

doi:10.1016/j.cca.2008.01.004

Cited by 28 publications

(24 citation statements)

References 31 publications

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“…Similar results were revealed by studies done on Slovakian men having episodes of MI (Bucova et al, 2009). However, in a study done on MI patients from Tunisia population showed a significant but not independent association of MCP-1 -2518 G-allele with MI ( Jemaa et al, 2008). In the present study, although statistically significant association was not observed in comparison of CAD and controls, but a trend towards higher G allele in CAD cases, especially, the GG homozygotes has been observed.…”

Section: Kaur Et Alcontrasting

confidence: 37%

Association of −2518A>G Promoter Polymorphism in the Monocyte Chemoattractant Protein-1 (MCP-1) Gene with Type 2 Diabetes and Coronary Artery Disease

Kaur

Matharoo

Arora³

et al. 2013

Genetic Testing and Molecular Biomarkers

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Aims: Inflammatory markers play an important role in the development of diseases related to metabolic syndrome, such as type 2 diabetes (T2D) and coronary artery disease (CAD). The present study evaluates the association of -2518A > G polymorphism in the monocyte chemoattractant protein-1 (MCP-1) gene with T2D and CAD. Results: The frequency of the G allele is greater in CAD cases (35%) as compared to T2D (24.6%) and controls (31%), while the frequency of the A allele is higher in T2D cases (75.4%) as compared to CAD cases (65%) and controls (69%). The analysis has revealed that in comparison to T2D cases, the G allele increases the risk of CAD by 1.9-fold ( p = 0.008; odds ratio [OR] = 1.9, 1.18-3.06 at 95% confidence interval [CI]) but in comparison to controls the G-allele provided protection against T2D ( p = 0.011; OR = 0.55, 0.35-0.87 at 95% CI), both under the dominant model (AG + GG vs. AA). Conclusion: Results of the present study suggests that G-allele of MCP-1 -2518A > G polymorphism is associated with reduced risk of T2D and increased risk of CAD in the population of Punjab. The results indicate that there is a difference in the association of risk alleles with phenotypes of metabolic syndrome. Body mass index and waist circumference are important risk factors for T2D in the population of Punjab.

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Section: Kaur Et Alcontrasting

confidence: 37%

Association of −2518A>G Promoter Polymorphism in the Monocyte Chemoattractant Protein-1 (MCP-1) Gene with Type 2 Diabetes and Coronary Artery Disease

Kaur

Matharoo

Arora³

et al. 2013

Genetic Testing and Molecular Biomarkers

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“…A strong link was found between CCL2 polymorphism and autoimmune diseases. CCL2 (-2518 A/G) single nucleotide polymorphism has been shown to be associated with the chronic stable angina pectoris [23], and a significant but not independent association was observed between the (-2518G/A) polymorphism of the CCL2 gene and myocardial infarction [24]. This single nucleotide polymorphism has also been shown to be involved with pulmonary sarcoidosis [25].…”

Section: Introductionmentioning

confidence: 99%

CC-chemokine ligand 2 inhibition in idiopathic pulmonary fibrosis: a phase 2 trial of carlumab

et al. 2015

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The objective of this study was to determine the safety and efficacy of carlumab in the treatment of idiopathic pulmonary fibrosis (IPF).A phase 2, randomised, double-blind placebo-controlled dose-ranging study was conducted in patients with IPF (n=126). Patients were randomised to carlumab (1 mg·kg −1 , 5 mg·kg, or 15 mg·kg −1 ) or placebo every 4 weeks. The primary endpoint was the rate of percentage change in forced vital capacity (FVC). Secondary endpoints were time to disease progression, absolute change in FVC, relative change in diffusing capacity of the lung for carbon monoxide (DLCO), and St George's Respiratory Questionnaire (SGRQ) total score.Due to a pre-planned, unfavourable interim benefit-risk analysis, dosing was suspended. The rate of percentage change in FVC showed no treatment effect (placebo −0.582%, 1 mg·kg −1 −0.533%, 5 mg·kg −1 −0.799% and 15 mg·kg −1 −0.470%; p=0.261). All active treatment groups showed a greater decline in FVC (1 mg·kg −1 −290 mL, 5 mg·kg −1 −370 mL and 15 mg·kg −1 −320 mL) compared with placebo (−130 mL). No effect on disease progression, DLCO, infection rates or mortality was observed. SGRQ scores showed a nonsignificant trend toward worsening with active treatment. Unexpectedly, free CC-chemokine ligand 2 levels were elevated above baseline at both 24 and 52 weeks. A higher proportion of patients with one or more serious adverse events was observed in the 5 mg·kg −1 group (53.1%) compared with 1 mg·kg −1 (15.2%), 15 mg·kg −1 (21.9%) and placebo (46.4%), although no unexpected serious adverse events were noted. Although dosing was stopped prematurely, it is unlikely that carlumab provides benefit to IPF patients. @ERSpublications It is unlikely that carlumab provides benefit to patients with idiopathic pulmonary fibrosis

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“…The study, which is based on the analysis of 13 studies (Szalai et al, 2001;Simeoni et al, 2004;Cermakova et al, 2005;McDermott et al, 2005;Bjarnadottir et al, 2006;Bucova et al, 2008;Cam et al, 2008;Jemaa et al, 2008;Bucova et al, 2009aBucova et al, , 2009bZhang et al, 2009;van Wijk et al, 2010;Zhong et al, 2010), found a probable increase in CAD with the MCP-1 -2518G allele in a population of Caucasian. However, the result might have been caused by publication bias and insufficient sample size.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, one case-only study (Alioglu et al, 2009) and two family-based studies (McGlinchey et al, 2004;Kim et al, 2007) were also excluded. Finally, 21 studies (Szalai et al, 2001;Simeoni et al, 2004;Cermakova et al, 2005;McDermott et al, 2005;Bjarnadottir et al, 2006;Iwai et al, 2006;Cam et al, 2008;Bucova et al, 2008;Jemaa et al, 2008;Bucova et al, 2009a;Bucova et al, 2009b;Zhang et al, 2009;Zhong et al, 2010;van Wijk et al, 2010;El Mahgoub et al, 2011;Lin et al, 2012;Wang & Zhang, 2012;Yang et al, 2012;Xu et al, 2013;Kaur et al, 2013;Nasibullin et al, 2014) with a total of 8,735 cases and 12,300 controls were included in this meta-analysis. The process of the study selection and exclusion is shown in Figure 1.…”

Section: Eligible Studies Included In the Meta-analysismentioning

confidence: 99%

Association of Monocyte Chemoattractant Protein‐1 (MCP‐1)‐2518A>G Polymorphism with Susceptibility to Coronary Artery Disease: A Meta‐Analysis

Bai

Wang

et al. 2015

Annals of Human Genetics

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SummaryWe attempted to systematically elucidate the association between monocyte chemoattractant protein-1 (MCP-1) -2518A>G polymorphism and risk of coronary artery disease (CAD). Eligible studies were identified through PubMed, EBSCO, and Web of Science Databases. The magnitude of MCP-1 polymorphism effect and its possible mode of action on CAD were estimated. The odds ratio (OR) with 95% confidence intervals (CI) were pooled in a specific genetic model to assess the association. A total of 21 studies were involved. There was significant gene effect on CAD risk in the overall population (likelihood ratio test: p < 0.0001). Patients with GG and AG genotypes had 1.435 (95% CI: 1.183-1.740) and 1.087 (95% CI: 1.008-1.172) times higher risk of CAD than those with AA genotype. These gene effects suggested a recessive model to be appropriate. The pooled OR was 1.362 (95% CI: 1.137-1.631; p uncorrected = 0.001, p FDR = 0.005) in the recessive model. In the ethnicity-stratified analysis, significant association was observed in the Caucasian population (OR = 1.492; 95% CI: 1.106-2.014; p uncorrected = 0.009, p FDR = 0.015), whereas no statistical significant association was detected in the Asian population (adjusted p = 0.124). The results suggested that MCP-1 -2518A>G polymorphism may be associated with susceptibility to CAD, especially in Caucasians.

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Association between the −2518G/A polymorphism in the monocyte chemoattractant protein-1 (MCP-1) gene and myocardial infarction in Tunisian patients

Cited by 28 publications

References 31 publications

Association of −2518A>G Promoter Polymorphism in the Monocyte Chemoattractant Protein-1 (MCP-1) Gene with Type 2 Diabetes and Coronary Artery Disease

Association of −2518A>G Promoter Polymorphism in the Monocyte Chemoattractant Protein-1 (MCP-1) Gene with Type 2 Diabetes and Coronary Artery Disease

CC-chemokine ligand 2 inhibition in idiopathic pulmonary fibrosis: a phase 2 trial of carlumab

Association of Monocyte Chemoattractant Protein‐1 (MCP‐1)‐2518A>G Polymorphism with Susceptibility to Coronary Artery Disease: A Meta‐Analysis

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