Gene-specific DNA methylation profiles and LINE-1 hypomethylation are associated with myocardial infarction risk

Guarrera, Simonetta; Fiorito, Giovanni; Onland‐Moret, N. Charlotte; Russo, Alessia; Agnoli, Claudia; Allione, Alessandra; Gaetano, Cornelia Di; Mattiello, Amalia; Ricceri, Fulvio; Chiodini, Paolo; Polidoro, Silvia; Frasca, Graziella; Verschuren, Monique; Boer, Jolanda M. A.; Iacoviello, Licia; Schouw, Yvonne T. van der; Tumino, Rosario; Víneis, Paolo; Krogh, Vittorio; Panico, Salvatore; Sacerdote, Carlotta; Matullo, Giuseppe

doi:10.1186/s13148-015-0164-3

Cited by 62 publications

(67 citation statements)

References 60 publications

(61 reference statements)

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“…A previous study showed that genetic factors are associated with age at stroke onset and sex [47]. Gene-specific DNA methylation profiles and LINE-1 hypomethylation are associated with myocardial infarction risk [48]. Recently, there was an attempt to find predictors of myocardial infarction using genotype/allelic combinations by analysis of genotype frequencies of polymorphic markers [49].…”

Section: Discussionmentioning

confidence: 99%

Promoter Polymorphism (-174, G/C) of Interleukin-6 and Arterial Thromboembolic Events: A Meta-Analysis

2016

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BackgroundIschemic stroke and myocardial infarction are fatal diseases and are among the top 10 causes of death in Korea, including arterial thromboembolic events. Many previous studies have described the function of interleukin-6 (IL-6) in arterial thromboembolic events and the association between promoter single-nucleotide polymorphism (SNP) (rs1800795; −174, G/C) of the IL-6 gene. However, these results were controversial. Therefore, we performed a meta-analysis to more precisely assess the association between the SNP of the IL-6 gene and susceptibility to arterial thromboembolic events.Material/MethodsWe used PubMed, Embase, Google Scholar, and Korean Studies Information Service System (KISS) electronic databases. Comprehensive Meta-analysis software (Corporation, NJ) was used to evaluate the relationship between rs1800795 SNP of IL-6 gene and risk of arterial thromboembolic events. Odds ratio (OR), 95% confidence interval (CI), and P value were also calculated. The 13 eligible studies were analyzed in the meta-analysis.ResultsThe present meta-analysis found that rs1800795 SNP of IL-6 gene is not significantly associated with susceptibility to arterial thromboembolic events (C allele vs. G allele, OR=1.04, 95% CI=0.91–1.19, P=0.619; CC vs. CG+GG, OR=1.09, 95% CI=0.91–1.31, P=0.364; CC+CG vs. GG, OR=0.97, 95% CI=0.78–1.21, P=0.763, respectively), and the SNP of IL-6 gene also did not show any significant association with ischemic stroke or myocardial infarction (P>0.05 in each model).ConclusionsWe found that rs1800795 SNP of IL-6 gene was not related to arterial thromboembolic events. However, further study will be needed to confirm these results.

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Section: Discussionmentioning

confidence: 99%

Promoter Polymorphism (-174, G/C) of Interleukin-6 and Arterial Thromboembolic Events: A Meta-Analysis

2016

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“…Guarrera et al found differential methylation of the zinc finger and Broad complex, Tramtrak, Bric à brac (BTB) domain-containing protein 12 ( ZBTB12 ) gene body and LINE-1 hypo-methylation in 291 cases of myocardial infarction vs. 292 controls from a large Italian European Prospective Investigation in to Cancer and Nutrition Study (EPICOR). 51 Replication in a second cohort, demonstrated that including DNA methylation profile with other traditional CVD risk factors may improve risk prediction. 51 CVD has also been associated with DNA methylation changes in response to a number of environmental factors, including air pollution.…”

Section: Health Outcomes and Dna Methylationmentioning

confidence: 99%

“…51 Replication in a second cohort, demonstrated that including DNA methylation profile with other traditional CVD risk factors may improve risk prediction. 51 CVD has also been associated with DNA methylation changes in response to a number of environmental factors, including air pollution. Recently, Zhong et.…”

Section: Health Outcomes and Dna Methylationmentioning

confidence: 99%

Epigenetics and Health Disparities

Vick

Burris

2017

Curr Epidemiol Rep

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Purpose of review African Americans disproportionately suffer from leading causes of morbidity and mortality including cardiovascular disease (CVD), cancer, and preterm birth. Disparities can arise from multiple social and environmental exposures, but how the human body responds to these exposures to result in pathophysiologic states is incompletely understood. Recent findings Epigenetic mechanisms, particularly DNA methylation, can be altered in response to exposures such as air pollution, psychosocial stress, and smoking. Each of these exposures has been linked to the above health states (CVD, cancer, and preterm birth) with striking racial disparities in exposure levels. DNA methylation patterns have also been shown to be associated with each of these health outcomes. Summary Whether DNA methylation mediates exposure-disease relationships and can help explain racial disparities in health is not known. However, because many environmental and adverse social exposures disproportionately affect minorities, understanding the role that epigenetics plays in the human response to these exposures that often result in disease, is critical to reducing disparities in morbidity and mortality.

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“…However, DNA methylation at MTHFR has not been examined to any great extent in relation to hypertension generally. Aberrant LINE-1 and gene-specific DNA methylation profiles have been reported to improve the prediction accuracy of the occurrence of myocardial infarction, when other well-known risk factors for hypertension are taken into account [70]. One randomised controlled trial found that B-vitamin supplementation (folic acid, vitamins B6 and B12) in combination with vitamin D and calcium, increased LINE-1 DNA methylation, but this study did not account for different MTHFR genotypes [71].…”

Section: Biological Mechanisms Linking Blood Pressure With One-carmentioning

confidence: 99%

Novel Approaches to Investigate One-Carbon Metabolism and Related B-Vitamins in Blood Pressure

et al. 2016

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Hypertension, a major risk factor for heart disease and stroke, is the world’s leading cause of preventable, premature death. A common polymorphism (677C→T) in the gene encoding the folate metabolizing enzyme methylenetetrahydrofolate reductase (MTHFR) is associated with increased blood pressure, and there is accumulating evidence demonstrating that this phenotype can be modulated, specifically in individuals with the MTHFR 677TT genotype, by the B-vitamin riboflavin, an essential co-factor for MTHFR. The underlying mechanism that links this polymorphism, and the related gene-nutrient interaction, with hypertension is currently unknown. Previous research has shown that 5-methyltetrahydrofolate, the product of the reaction catalysed by MTHFR, appears to be a positive allosteric modulator of endothelial nitric oxide synthase (eNOS) and may thus increase the production of nitric oxide, a potent vasodilator. Blood pressure follows a circadian pattern, peaking shortly after wakening and falling during the night, a phenomenon known as ‘dipping’. Any deviation from this pattern, which can only be identified using ambulatory blood pressure monitoring (ABPM), has been associated with increased cardiovascular disease (CVD) risk. This review will consider the evidence linking this polymorphism and novel gene-nutrient interaction with hypertension and the potential mechanisms that might be involved. The role of ABPM in B-vitamin research and in nutrition research generally will also be reviewed.

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Gene-specific DNA methylation profiles and LINE-1 hypomethylation are associated with myocardial infarction risk

Cited by 62 publications

References 60 publications

Promoter Polymorphism (-174, G/C) of Interleukin-6 and Arterial Thromboembolic Events: A Meta-Analysis

Promoter Polymorphism (-174, G/C) of Interleukin-6 and Arterial Thromboembolic Events: A Meta-Analysis

Epigenetics and Health Disparities

Novel Approaches to Investigate One-Carbon Metabolism and Related B-Vitamins in Blood Pressure

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