<b><i>NT5C2</i></b> Gene Polymorphisms and the Risk of Coronary Heart Disease

Abstract

Background: Increasing studies have reported that 5′-nucleotidase cytosolic II (NT5C2) has a strong relationship with coronary heart disease (CHD) development. This study was designed to examine the relationship between NT5C2 polymorphisms and CHD in the Chinese Han population. Methods: We studied 501 CHD patients and 496 healthy controls from the Second Affiliated Hospital of Hainan Medical University in Hainan Province, China. Four single nucleotide polymorphisms (SNPs) in NT5C2 were selected and genotyped using Agena MassARRAY technology. Odds ratios and 95% confidence intervals were calculated using logistic regression after adjusting for age and gender. Stratification analysis was performed by age and gender in all individuals; we especially investigated the effects of NT5C2 SNPs on hypertension and diabetes among CHD patients. Results: rs2148198 of NT5C2 was strongly associated with an increased risk of CHD (allele: p = 0.045; codominant: p = 0.007; additive: p = 0.016). Stratified analysis revealed that rs2148198 was associated with increased CHD risk in individuals aged ≤61 years and males. For CHD patients, rs2148198 significantly affected the risk of hypertension and diabetes (p < 0.05). Further, rs79237883 of NT5C2 was associated with decreased susceptibility to hypertension in multiple genetic models for individuals with CHD (allele: p = 0.007; codominant: p = 0.001; dominant: p = 0.001; additive: p = 0.008). Conclusion: This study reports the association of NT5C2 gene variants and CHD susceptibility in the Chinese Han population. Especially, NT5C2 rs2148198 was significantly associated with CHD risk in the subgroups of males, hypertension, and diabetes.

Rs420137, rs386360 and rs7763726 polymorphisms in fibronectin type III domain containing 1 are associated with susceptibility to coronary heart disease: Analysis in the Han population

“…At the same time, these three SNPs increased the risk of CHD in patients aged 62 years and younger and smokers. These results are consistent with previous studies indicating that genetic polymorphisms influence the susceptibility to CHD in males or patients aged ≤61 years ( 29 , 30 ). Zhao et al ( 31 ) found that the morbidity and mortality of cardiovascular diseases were correlated with the degree of blood pressure elevation.…”

The effect of CYP7B1 polymorphisms on the risk of coronary heart disease in Hainan Han population

“…CHD is a kind of multifactorial disease resulting from environmental and genetic factor. An increasing number studies strongly supported that genetic polymorphisms involve in the risk of CHD, such as SCARB1 [ 26 ], RTEL1 [ 27 ], 5- HTTLPR [ 28 ], CD40 [ 29 ], and NT5C2 [ 30 ]. The CYP7B1 gene is located on chromosome 8q21.3.…”

“…Similar to our findings, Zhang et al and Ye et al reported that genetic polymorphism influence CHD risk in age > 60 years and age > 65 years [ 31 , 32 ]. However, Huang et al and Chen et al showed that gene variants are associated with the susceptibility to CHD in age ≤ 61 years [ 30 , 33 ]. Age is a risk factor for CHD.…”

“…Our results seem to be consistent with other research which found genetic polymorphisms are associated with CHD risk in women [ 38 ]. In contrast, Luo et al, Ma et al, and Chen et al indicated that genetic polymorphisms affect the risk of CHD in men [ 26 , 30 , 39 ]. Gender is also a risk factor for CHD.…”

The ceRNA Crosstalk between mRNAs and lncRNAs in Diabetes Myocardial Infarction

“…PPP1R3G is downregulated in the liver by fasting and increased by feeding, and it plays an important role in the control of postprandial glucose homeostasis through its regulation of hepatic gluconeogenesis during the fasting–feeding transition [ 43 ]. The 5′-nucleotidase cytosolic II (NT5C2) variants were reported to be nominally associated with coronary heart disease (CHD) susceptibility in the subgroups of males and with hypertension and diabetes [ 44 ]. Ubiquitin-specific protease 15 (USP15) was found to be a potential target of miR-26a and mediated the proautophagic and cardioprotective effects of miR-26a against ischemic injury [ 45 ].…”