Balkan Journal of Medical Genetics

ASSOCIATION OF GENETIC POLYMORPHISMS IN THE Matrix Gla Protein (MGP) GENE WITH CORONARY ARTERY DISEASE AND SERUM MGP LEVELS
Karsli-Ceppioglu S1,*, Yazar S2, Keskin Y3, Karaca M4, Luleci NE3, Yurdun T1
*Corresponding Author: Seher Karsli-Ceppioglu, Ph.D., Department of Toxicology, Faculty of Pharmacy, Marmara University, Tibbiye Street No. 49, İstanbul 34668, Turkey. Tel: +90-216-414-2962. Fax: +90-216-345-2952. E-mail: seher.karsli@marmara.edu.tr
page: 43

MATERIALS AND METHODS

Sample Collection and Clinical Assessment. The study was conducted with 168 Caucasian participants recruited between February 2011 and November 2012 from the Cardiology Department of İstanbul Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, İstanbul, Turkey. Patients suspected of having CAD with health complaints such as angina, atypical chest pain and chest distress, were enrolled in the study. After general medical inquiry, routine blood and urine assays, patients admitted to the Department of Cardiology to determine the presence of concomitant CAD. Coronary angiography was performed in all subjects through the femoral artery by the Judkins technique to determine the presence of arterial calcification. One hundred and twelve of subjects were considered as CAD patients, who had at least one vessel with >50.0% narrowing of the luminal diameter. The CAD group was also divided into three subgroups as single-vessel disease (n = 62), two-vessel disease (n = 30) and three-vessel disease (n = 20), according to the number of main vessels with significant stenosis. Subjects who had normal coronary arteries, without cardiovascular disease, were enrolled as a control group (n = 56). Informed consent was provided by all volunteers who participated in the study. The study protocol was approved by the local ethics committee of Marmara University and Turkish Ministry of Health, Central Ethics Committee (ID: 09.2011.0020, 2011). The patients with malignancies were excluded. Demographic and clinical data, including underlying diseases such as hypertension and diabetes mellitus (DM), smoking, alcohol consumption and family history were collected from medical records. Biochemical data related with CAD, such as serum glucose, triglyceride, low density lipoprotein (LDL)-cholesterol, high density lipoprotein (HDL)-cholesterol, total cholesterol and creatinine, were assayed using routine clinical methods. Table 1 represents demographic and biochemical profiles of participants. Genotyping of MGP SNPs. Peripheral blood samples from participants were collected and then genomic DNA was extracted by Roche DNA isolation kit (Roche Diagnostics GmbH, Mannheim, Germany). The genotyping of rs1800802 (T138-C) in the promoter region, rs4236 (Thr83-Ala) and rs12304 (Glu60-X) in exon 4 of the MGP gene, was carried out using polymerase chain reaction (PCR), (CSL Gradient Thermal Cycler; Cleaver Scientific Ltd., Rugby, Warwickshire, UK). The location of the studied SNPs on a schematic representation of the MGP gene structure are shown in Figure 1. Genotyping of rs1800802 and rs4236 SNPs was performed by using PCR with subsequent restriction fragment length polymorphism (RFLP) analysis as previously reported by Garbuzova et al. [11]. Genotyping of rs12304 polymorphism was carried out as described previously [10]. Serum MGP Levels. Serum samples of participants were separated from whole blood and kept at –20 °C until they were analyzed. An enzyme-linked immunosorbent assay (ELISA) provided by Sunred Biological Technology (Shanghai, People’s Republic of China) was used to measure concentrations of serum MGP. Statistical Analyses. The statistical analyses were performed with the Statistical Package for the Social Sciences (SPSS®) software (version 20) (https://ibm. com/ SPSS-Statistics/Software). All results expressed as means ± SD and p value less than 0.05 were defined to be statistically significant. Hardy-Weinberg equilibrium (HWE) testing was executed to compare the monitored and expected genotype frequencies of subjects using the χ2 test. Descriptive statistics and multivariate analyses were performed to estimate the relationships between clinical profiles and MGP alleles. The results were adjusted for the cofounders age and gender. Multinomial logistic regression analysis was used to determine the odds ratio (OR) of the genotype for the occurrence of CAD. Linkage disequilibrium (LD) block structures of MGP gene SNPs, HWE test and calculation of haplotype frequencies and estimated associations between haplotypes and CAD risk were performed by Haploview (version 4.2) (https://www. broad institute.org/haploview/haploview) [12].

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