Elsevier

Clinical Biochemistry

Volume 46, Issue 12, August 2013, Pages 1047-1054
Clinical Biochemistry

A novel polymorphism of the CYP2J2 gene is associated with coronary artery disease in Uygur population in China

https://doi.org/10.1016/j.clinbiochem.2013.05.003Get rights and content
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Abstract

Background

Cytochrome P450 (CYP) 2J2 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs). The EETs are potent endogenous vasodilators and inhibitors of vascular inflammation. The aim of the present study was to assess the association between the human CYP2J2 gene polymorphism and coronary artery disease (CAD) in a Han and Uygur population of China.

Methods

We use two independent case–control studies: a Han population (206 CAD patients and 262 control subjects) and an Uygur population (336 CAD patients and 448 control subjects). All CAD patients and controls were genotyped for the same three single nucleotide polymorphisms (SNPs) (rs890293, rs11572223 and rs2280275) of CYP2J2 gene by a real-time PCR instrument.

Results

In the Uygur population, for total, the distribution of SNP3 (rs2280275) genotypes showed a significant difference between CAD and control participants (P = 0.048). For total and men, the distribution of SNP3 (rs2280275) alleles and the dominant model (CC vs CT + TT) showed a significant difference between CAD and control participants (for allele: P = 0.014 and P = 0.035, respectively; for dominant model: P = 0.014 and P = 0.034, respectively). The significant difference in dominant model was retained after adjustment for covariates (OR: 0.279, 95% confidence interval [CI]: 0.176–0.440, P = 0.001; OR: 0.240, 95% CI: 0.128–0.457, P = 0.001, respectively).

Conclusions

The CC genotype of rs2280275 in CYP2J2 gene could be a protective genetic marker of CAD and T allele may be a risk genetic marker of CAD in men of Uygur population in China.

Graphical abstract

Schematic of EET interactions with cardiovascularion channels.

A: In the cardiac myocyte, EETs activate sarcolemmal or mitochondrial KATP channels.

B: In the vasculature, EETs activate endothelial small (SKCa) or intermediate (IKCa) conductance calcium-activated channels to cause hyperpolarization, which can be transmitted to the vascular smooth muscle via myoendothelial gap junctions. EETs also activate TRPV4 channels to activate Ca2 + influx. In the vascular smooth muscle, EETs activate large conductance, calcium-activated (BKCa) channels through a G-protein-coupled event.

C: In platelets, EETs activate BKCa channels

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Keywords

CYP2J2
Single nucleotide polymorphism
Coronary artery disease
Case–control study

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These authors contributed equally to this work.