CDKN2A and CDKN2B methylation in coronary heart disease cases and controls

Zhong, Jinyan; Chen, Xiaoying; Ye, Huadan; Wu, Nan; Chen, Xiaomin; Duan, Shiwei

doi:10.3892/etm.2017.5310

Cited by 5 publications

(4 citation statements)

References 39 publications

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“…Однако интересно, что, например, в метаанализе исследований метилирования гена при раке пищевода в большинстве исследований в контрольной группе (без рака) ген CDKN2A также не был метилирован у большинства участников (материалом для исследования служила кровь или ткань пищевода) [12]. В исследовании «случай-контроль» в Китае не выявлено ассоциации метилирования гена CDKN2A с ИБС, доля образцов с метилированным геном CDKN2A составляла 15-20 % [13]. Таким образом, отсутствие гена в CDKN2A в метилированном состоянии в настоящем исследовании может быть связано с небольшими размерами исследуемых групп, расовыми особенностями изучаемых лиц, особенностями метилирования гена в ткани миокарда.…”

Section: Discussionunclassified

Methylation of F2RL3, CDKN2A genes and sudden cardiac death

Иванова

Gurazheva

Maksimova

et al. 2022

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The aim of the study was to evaluate the association of methylation of the F2RL3, CDKN2A gene with sudden cardiac death (SCD). Material and methods. Case-control study design. The SCD group included 150 deceased men (mean age 46.7 ± 9.2 years) with the main pathological diagnoses of acute circulatory failure, acute coronary insufficiency, which meets the SCD criteria of the European Society of Cardiology. The control group included 150 men who died suddenly, but not due to cardiovascular pathology (mean age 42.6 ± 1.2 years). DNA was isolated by phenol-chloroform extraction from myocardial tissue in both groups. The methylation status of the F2RL3 gene (19: 16890405-16890606, GRCh38.p13) and the CDKN2A gene (9: 21974726-21974877, GRCh38.p13) was assessed by methyl-specific polymerase chain reaction. Results. In the SCD group, 17.3 % (26/150) had the F2RL3 gene completely methylated (MM); in 6.0 % (9/150) it is completely unmethylated (UU); 76.7 % (115/150) had both methylated and unmethylated F2RL3 (MU) gene. In the control group, 16 % (24/150) had the F2RL3 gene completely methylated (MM); in 5.3 % (8/150), it is completely unmethylated (UU); 78.7 % (118/150) had both methylated and unmethylated F2RL3 (MU) gene. When comparing the groups, there were no statistically significant differences in the methylation status of the F2RL3 gene between the groups (p > 0.05). In all subjects in the SCD group and the control group, the CDKN2A gene is completely unmethylated. Conclusions. Methylation of genes F2RL3, CDKN2A is not associated with sudden cardiac death.

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Section: Discussionunclassified

Methylation of F2RL3, CDKN2A genes and sudden cardiac death

Иванова

Gurazheva

Maksimova

et al. 2022

jour

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“…Sex dimorphism of CHD has been observed in the prevalence and the onset age of CHD (21,41). Notably, the onset age of CHD in women is typically 10 years later than that in men (21).…”

Section: Discussionmentioning

confidence: 99%

Elevated methylation of cyclin dependent kinase inhibitor 2B contributes to the risk of coronary heart disease in women

Chen

Jiang

et al. 2018

Exp Ther Med

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Cyclin dependent kinase inhibitor 2B (CDKN2B) encodes a cyclin-dependent kinase inhibitor that may enhance the formation of atherosclerotic plaques. The aim of the present study was to investigate the contribution of CDKN2B promoter methylation on the risk of coronary heart disease (CHD). The present results indicated a significant association between increased CDKN2B methylation and the risk of CHD (adjusted P=0.043). A breakdown analysis according to sex demonstrated that CDKN2B methylation was significantly associated with the risk of CHD in women (adjusted P=0.010), but not in men. A further breakdown analysis by age indicated a significant association of CHD in the women >60 years (P=0.024). Luciferase reporter gene assay results indicated that the CDKN2B promoter fragment significantly enhanced luciferase activity (P<0.001). In addition, CDKN2B transcription was significantly enhanced following treatment with 5-aza-2′-deoxycytidine methylation inhibitor in human aortic endothelial cells (HAEC) and human primary coronary artery smooth muscle cells (HPCASMC; P<0.05 and P<0.01), but not in 293 cells. Notably, estrogen treatment reduced CDKN2B methylation of several CpGs and significantly increased CDKN2B gene expression levels in HAEC, HPCASMC and 293 cells (P<0.05 and P<0.01). Additionally, treatment of HAEC and HPCASMC with simvastatin and γ-carboxy-L-glutamic acid reduced CDKN2B promoter methylation and increased CDKN2B transcription concomitantly. The present study suggests that CDKN2B promoter methylation may be associated with sex dimorphism in the pathogenesis of CHD.

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“…Negative regulator of insulin activity [28] Generalized arterial calcification of infancy [78] Hypophosphatemic rickets [78] India (Punjab, Orissa, Jammu and Kashmir) [54] Europeans [28] 13 Alpha-Ketoglutarate-Dependent Dioxygenase (FTO) encodes for a non-heme and 2-oxoglutaratedependent oxygenase with nucleic acid demethylase activity [58] Obesity [26] Obesity related Hypertension [79] Colon cancer [80] India (Punjab, Orissa, Jammu and Kashmir, Chennai) [26,54] 14 Cyclin-Dependent Kinase Inhibitor 2B CDKN2B Regulation of beta-cell mass, proliferation and insulin secretory function [81] Glaucoma [82] Coronary artery disease [83] UK population [27] 15 Solute Carrier Family 16 Member 11 (SLC16A11) Hepatic liver metabolism [84] Type 2 diabetes [84] UK population [26] 16 Dual specificity phosphatase 9 (DUSP9) Susceptibility to insulin resistance [85] Prediabetes [19] Gestational diabetes mellitus [85] European population [19] 17 Kruppel-like factor 14 (KLF14)…”

Section: Insulin-degrading Enzyme (Ide)mentioning

confidence: 99%

Genetics of type 2 diabetes mellitus in Indian and Global Population: A Review

Joseph

Thirupathamma

Sathish

et al. 2022

Egypt J Med Hum Genet

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Background Non-communicable diseases such as cardiovascular diseases, respiratory diseases and diabetes contribute to the majority of deaths in India. Public health programmes on non-communicable diseases (NCD) prevention primarily target the behavioural risk factors of the population. Hereditary is known as a risk factor for most NCDs, specifically, type 2 diabetes mellitus (T2DM), and hence, understanding of the genetic markers of T2DM may facilitate prevention, early case detection and management. Main body We reviewed the studies that explored marker–trait association with type 2 diabetes mellitus globally, with emphasis on India. Globally, single nucleotide polymorphisms (SNPs) rs7903146 of Transcription Factor 7-like 2 (TCF7L2) gene was common, though there were alleles that were unique to specific populations. Within India, the state-wise data were also taken to foresee the distribution of risk/susceptible alleles. The findings from India showcased the common and unique alleles for each region. Conclusion Exploring the known and unknown genetic determinants might assist in risk prediction before the onset of behavioural risk factors and deploy prevention measures. Most studies were conducted in non-representative groups with inherent limitations such as smaller sample size or looking into only specific marker–trait associations. Genome-wide association studies using data from extensive prospective studies are required in highly prevalent regions worldwide. Further research is required to understand the singular effect and the interaction of genes in predicting diabetes mellitus and other comorbidities.

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CDKN2A and CDKN2B methylation in coronary heart disease cases and controls

Cited by 5 publications

References 39 publications

Methylation of F2RL3, CDKN2A genes and sudden cardiac death

Methylation of F2RL3, CDKN2A genes and sudden cardiac death

Elevated methylation of cyclin dependent kinase inhibitor 2B contributes to the risk of coronary heart disease in women

Genetics of type 2 diabetes mellitus in Indian and Global Population: A Review

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