The -308G/A of Tumor Necrosis Factor (TNF)-α and 825C/T of Guanidine Nucleotide Binding Protein 3 (GNB3) are Associated with the Onset of Acute Myocardial Infarction and Obesity in Taiwan

Chang, Wei-To; Wang, Yicheng; Chen, Chun-Chang; Zhang, Shikun; Liu, Chen-Hsun; Chang, Fu‐Hsin; Hsu, Li‐Sung

doi:10.3390/ijms13021846

Cited by 21 publications

(13 citation statements)

References 37 publications

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“…Chang et al also proved that TNF-a-308 G>A gene polymorphism was associated with obesity, 11 whereas Sobti et al reported that the AA and GA genotypes of TNF-a 308 G>A were associated with a higher risk of obesity in men; in women, only the AG genotype was associated with a higher risk of developing this nutritional disorder. The AA and GA homozygotes were also observed to present a higher risk for developing obesity-associated metabolic syndromes.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, Chang proved that TNF-a 308 G/A polymorphism is associated with obesity. 11 Based on the above-mentioned hypotheses, by using BMI as a relevant indicator of nutritional status, the present research aimed: i) to determine whether TNF-a 308G>A gene polymorphism is associated with overweight status, ii) to determine whether TNF-a 308G>A gene polymorphism is related to anthropometric (body mass index (BMI), mid-upper arm circumference (MUAC), and tricipital skinfold thickness (TST)) and biochemical (proteins, cholesterol, triglycerides, and lipids) variables, and iii) to quantify the influence of the studied gene polymorphism on overweight risk in children by assessing certain laboratory variables (cholesterol, LDL cholesterol, aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), and glycemia (Gly).…”

Section: Introductionmentioning

confidence: 99%

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The impact of TNF-α 308G>A gene polymorphism on children’s overweight risk and an assessment of biochemical variables: A cross-sectional single-center experience

Mărginean

Iancu²,

Moldovan

et al. 2019

Pediatrics & Neonatology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The impact of TNF-α 308G>A gene polymorphism on children’s overweight risk and an assessment of biochemical variables: A cross-sectional single-center experience

Mărginean

Iancu²,

Moldovan

et al. 2019

Pediatrics & Neonatology

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“…Controversially, Chang et al [29] and El Naggar et al [30] suggested that TNF-α-308 A>G is associated with increased risk of CAD and MI with other metabolic diseases like obesity and type 2 diabetes mellitus. They explained that the G to A substitute of -308 nucleotide located in the promoter region of the TNF-α gene alters its mRNA transcription level and contributes to raise TNF-α secretion in serum.…”

Section: Discussionmentioning

confidence: 99%

Association of Tumor necrosis factor G-308 A Polymorphism and Its Correlation with Inflammatory Markers and Lipid Profile in Coronary Heart Disease.

Patil¹

2018

Int J Med Biochem

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C oronary heart disease (CHD) is defined as acute or chronic cardiac disability caused by imbalance between the myocardial supply and demand for oxygenated blood [1]. Cardiovascular disorders (CVD) are the leading cause of morbidity and mortality. CVD will be the most important cause of mortality in India, and CHD will be the single most vital source to this increasing burden of CVD [2]. According to World Health Organization (WHO), CHD is a modern epidemic, not an unavoidable attribute of aging [3]. The burden of CHD is rising in India. In 2008, CHD caused 7.2 million deaths (i.e., 12.8% of total deaths) [4]. In the etiology, CHD is caused by any disease affecting the coronary arteries. More than 90% cases were caused by coronary atherosclerosis and 10% by other causes like vasospasm, Objectives: Tumor necrosis factor-alpha (TNF-α) is a primary proinflammatory cytokine. Single nucleotide polymorphisms present in the promoter region of cytokines have been implicated in the cardiovascular disease pathogenesis. Thus, this study aims to understand the role of permissive promoter variants in TNF-α G-308 A and its correlation with inflammatory markers and lipid profile in the coronary heart disease. Methods: We determined the genotyping of TNF-α G-308 A polymorphism by allele-specific polymerase chain reaction assay in 109 cases with coronary heart disease and 120 controls. Allele and genotype frequencies were estimated. The strength of the association of TNF-α-308 G >A and risk of coronary heart diseases was measured by odds ratios (ORs) and 95% confidence interval. Results: In coronary heart disease and controls, the frequencies of minor allele TNF-α-308 "A" were 0.190 and 0.158, respectively, while the frequencies of major allele TNF-α "G" were 0.809 and 0.841, respectively. The genotype frequencies of TNF-α-308 G-A in coronary heart disease cases were GG=68.81%, GA=26.61%, AA=4.58%; and the frequencies in controls were GG=76.67%, GA=20.83%, AA=2.50%. The OR for wild related to the TNF-α polymorphism was 0.6714 (0.3737-1.206; p=0.233). The OR for heterozygous was 1.387 (0.7468-2.541 p=0.350), and the OR for homozygous was 1.857 (0.4372-8.041 p=0.482). The differences in AA genotype frequencies of TNF-α-308 G-A between cases and controls have led to an OR 1.857; 0.4372-8.041; p=0.4829 in the univariate analysis that was not significant. Conclusion: No association was observed between the permissive promoter variants in the TNF-α gene and an increased risk of coronary heart disease.

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“…TNF-α is a multifunctional cytokine; as a key inflammatory mediator of AMI, TNF-α has been the subject of increased research. Animals overexpressing TNF suffer from severe heart disease, including arrhythmia (26)(27)(28). This indicates that upregulation of TNF expression is closely associated with the dysfunction of cardiac myocytes (29,30).…”

Section: Discussionmentioning

confidence: 99%

Effect of lysophosphatidic acid on the immune inflammatory response and the connexin 43 protein in myocardial infarction

Zhang

Zhao

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Lysophosphatidic acid (LPA) is an intermediate product of membrane phospholipid metabolism. Recently, LPA has gained attention for its involvement in the pathological processes of certain cardiovascular diseases. The aim of the present study was to clarify the association between the effect of LPA and the immune inflammatory response, and to investigate the effects of LPA on the protein expression levels of connexin 43 during myocardial infarction. Surface electrocardiograms of myocardial infarction rats and isolated rat heart tissue samples were obtained in order to determine the effect of LPA on the incidence of arrhythmia in rats that exhibited changes in immune status. The results demonstrated that the incidence of arrhythmia decreased when the rat immune systems were suppressed, and the incidence of arrhythmia increased when the rat immune systems were enhanced. The concentration levels of tumor necrosis factor (TNF)-α were determined by ELISA, and the results demonstrated that LPA induced T lymphocyte synthesis and TNF-α release. Using a patch-clamp technique, LPA was shown to increase the current amplitude of the voltage-dependent potassium channels (K v ) and calcium-activated potassium channels (K Ca ) in Jurkat T cells. The protein expression of connexin 43 (Cx43) was determined by immunohistochemical staining. The results indicated that LPA caused the degradation of Cx43 and decreased the expression of Cx43. This effect was associated with the immune status of the rats. There was a further decrease in Cx43 expression in the rats of the immune-enhanced group. To the best of our knowledge, these results provide the first evidence that LPA causes arrhythmia through the regulation of immune inflammatory cells and the decrease of Cx43 protein expression. The present study provided an experimental basis for the treatment of arrhythmia and may guide clinical care. IntroductionAcute myocardial infarction (AMI) is a disease that severely affects the health and life quality of patients. Arrhythmia is a complication of myocardial infarction, which is one of the most severe cardiovascular diseases, and it is the predominant cause of myocardial infarction-associated mortality (1). Since patients with ischemic heart disease are particularly prone to arrhythmias, they are often admitted for arrhythmia monitoring (2). Lysophosphatidic acid (LPA), which is an intermediate product of membrane phospholipid metabolism, is a lipid mediator with various biological functions that are predominantly mediated by specific G protein-coupled receptors (3). As a water-soluble glycerol phospholipid with a simple structure, LPA is secreted from numerous cell types, including platelets, fibroblasts and ovarian cancer cells (4). The concentration of LPA in regional myocardial tissue and plasma increases during myocardial infarction, and it can also cause arrhythmia (5).During myocardial infarction, both the infarcted area and the non-infarcted area exhibit perivasculitis, and the infiltration of a large number of inflammator...

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The -308G/A of Tumor Necrosis Factor (TNF)-α and 825C/T of Guanidine Nucleotide Binding Protein 3 (GNB3) are Associated with the Onset of Acute Myocardial Infarction and Obesity in Taiwan

Cited by 21 publications

References 37 publications

The impact of TNF-α 308G>A gene polymorphism on children’s overweight risk and an assessment of biochemical variables: A cross-sectional single-center experience

The impact of TNF-α 308G>A gene polymorphism on children’s overweight risk and an assessment of biochemical variables: A cross-sectional single-center experience

Association of Tumor necrosis factor G-308 A Polymorphism and Its Correlation with Inflammatory Markers and Lipid Profile in Coronary Heart Disease.

Effect of lysophosphatidic acid on the immune inflammatory response and the connexin 43 protein in myocardial infarction

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