Lack of association between IL-1 and IL-6 gene polymorphisms and myocardial infarction in Turkish population.

Yazan: admin Tarih: Oca 25th, 2011 | Kategori:: myocardial infarction

Int J Immunogenet. 2011 Jan 4. doi: 10.1111/j.1744-313X.2010.00988.x.

Coker A, Arman A, Soylu O, Tezel T, Yildirim A.

The Faculty of Science and Letters, Istanbul Kultur University, Istanbul, Turkey The Faculty of Engineering, Marmara University, Istanbul, Turkey The Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey.

Abstract

Inflammation and genetics play a key role in the pathogenesis of atherosclerosis and its clinical result myocardial infarction (MI). Proinflammatory cytokines, IL-1 and IL-6, have been shown to play essential roles in developmental stages of coronary artery plaque formation. The aim of this study was to determine the association between IL-1 [IL-1RN, IL-1β (-511, +3953)], IL-6 [-174, -572, -597] gene polymorphisms and MI in Turkish population. A total of 402 people were participated; 235 healthy control subjects and 167 MI patients (MI < 40, n: 72; MI > 40, n: 95). Polymerase chain reaction (PCR) was used to determine the genotype of IL-1RN, whereas the genotypes of IL-1β (-511, +3953) and IL-6 (-174, -572, -597) were determined using PCR followed with restriction digestion analysis. There was no significant difference between MI and controls for IL-1RN, IL-1β-511, +3953 (P: 0.875, 0.608, 0.442) and IL-6 -174, -572, -597 (P: 0.977, 0.632, 0.584) gene polymorphisms. Lack of association was observed between MI at younger age (MI < 40) and either IL-1RN VNTR, IL-1β-511, +3953 (P: 0.878, 0.732, 0.978) or IL-6 -174, -572, -597 (P: 0.313, 0.654, 0.552) gene polymorphisms. This study demonstrated that there was not any association between IL-1, IL-6 gene variants and MI in Turkish population. In addition, IL-1 and IL-6 gene polymorphisms did not affect MI at younger age (MI < 40) or older age (MI > 40). Thus, IL-1 and IL-6 single nucleotide polymorphisms may not be a risk factor for susceptibility to MI in Turkish population.


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Are PON1 Q/R 192 and M/L 55 polymorphisms risk factors for diabetes complications in Turkish population?

Yazan: admin Tarih: Oca 25th, 2011 | Kategori:: Diabetes Mellitus

Clin Biochem. 2011 Jan 9.

Altuner D, Suzen SH, Ates I, Koc GV, Aral Y, Karakaya A.

Ankara University, Faculty of Pharmacy, Department of Toxicology, 06100, Tandogan, Ankara, Turkey.

Abstract

OBJECTIVES: We investigated whether the human serum paraoxonase (PON1) Q/R 192 and M/L 55 polymorphisms are associated with the complications of the type 2 diabetes (T2D).

DESIGN AND METHODS: Study group was consisted of 50 healthy subjects and 100 type 2 diabetes mellitus (DM) patients. Following measuring of serum PON1 activity, isolation of DNA and genotyping analyses were performed.

RESULTS: PON1 activity of the patients with complications was significantly reduced by 23.5% compared to the group of diabetic patients and by 26.3% than the controls. According to multivariate analysis, we observed a three times significant effect of Q/R 192 polymorphism on the susceptibility to the occurrence of complications.

CONCLUSIONS: Protective effects of paraoxonase against peroxidation of LDL particles are important in T2D complications. Although both of the two polymorphisms are associated, 192 polymorphism seems to be stronger predictor of the risk of diabetic complications.


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The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery disease

Yazan: admin Tarih: Şub 25th, 2010 | Kategori:: Paraoxonase

Turk Kardiyol Dern Ars. 2009 Oct;37(7):473-8.

Taşkiran P, Cam SF, Sekuri C, Tüzün N, Alioğlu E, Altintaş N, Berdeli A.

Department of Medical Biology and Genetics, Medicine Faculty of Celal Bayar University, Manisa, Turkey.

OBJECTIVES: Paraoxonase (PON1) is a high-density lipoprotein (HDL)-associated esterase that hydrolyses lipoperoxides. PON1 serves as a protective factor against oxidative modification of LDL, suggesting that it may play an important role in the prevention of atherosclerotic process. Research has focused on two polymorphisms: leucine (L allele) to methionine (M allele) substitution at codon 55, and glutamine (A allele) to arginine (B allele) substitution at codon 192. STUDY DESIGN: We examined amino acid changes at codon 55 and 192 in the PON1 gene by polymerase chain reaction and using restriction enzymes in 120 patients (92 men, 28 women; mean age 48.2+/-4.3 years) with premature coronary artery disease (CAD) and in 102 healthy subjects (80 men, 22 women; mean age 46.8+/-5.2 years) with no history of CAD and a normal electrocardiogram. RESULTS: Distribution of genotypes in the patient and control groups at codon 55 were 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequency of genotypes at codon 192 were as follows: 4.2% and 2% for RR, 40% and 35.3% for QR, and 55.8% and 62.8% for QQ, respectively. While the frequency of PON1 55M allele was higher in the CAD group (0.3 vs. 0.2), PON1 192R allele frequency did not differ (p>0.05). There was a significant relationship between the PON1 M/L55 polymorphism and CAD (p=0.017), whereas the R/Q192 polymorphism was not associated with CAD (p=0.445). CONCLUSION: These data suggest that the PON1 M/L55 polymorphism shows a significant relationship with CAD and the Q/R192 polymorphism is not a major risk factor causing susceptibility to CAD in our population.


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The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery disease.]

Yazan: admin Tarih: Şub 3rd, 2010 | Kategori:: Paraoxanase gene

Turk Kardiyol Dern Ars. 2009;37(7):473-478.

Taşkıran P, Cam SF, Sekuri C, Tüzün N, Alioğlu E, Altıntaş N, Berdeli A.

Department of Medical Biology and Genetics, Medicine Faculty of Celal Bayar University, Manisa, Turkey.

OBJECTIVES: Paraoxonase (PON1) is a high-density lipoprotein (HDL)-associated esterase that hydrolyses lipoperoxides. PON1 serves as a protective factor against oxidative modification of LDL, suggesting that it may play an important role in the prevention of atherosclerotic process. Research has focused on two polymorphisms: leucine (L allele) to methionine (M allele) substitution at codon 55, and glutamine (A allele) to arginine (B allele) substitution at codon 192. STUDY DESIGN: We examined amino acid changes at codon 55 and 192 in the PON1 gene by polymerase chain reaction and using restriction enzymes in 120 patients (92 men, 28 women; mean age 48.2+/-4.3 years) with premature coronary artery disease (CAD) and in 102 healthy subjects (80 men, 22 women; mean age 46.8+/-5.2 years) with no history of CAD and a normal electrocardiogram. RESULTS: Distribution of genotypes in the patient and control groups at codon 55 were 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequency of genotypes at codon 192 were as follows: 4.2% and 2% for RR, 40% and 35.3% for QR, and 55.8% and 62.8% for QQ, respectively. While the frequency of PON1 55M allele was higher in the CAD group (0.3 vs. 0.2), PON1 192R allele frequency did not differ (p>0.05). There was a significant relationship between the PON1 M/L55 polymorphism and CAD (p=0.017), whereas the R/Q192 polymorphism was not associated with CAD (p=0.445). CONCLUSION: These data suggest that the PON1 M/L55 polymorphism shows a significant relationship with CAD and the Q/R192 polymorphism is not a major risk factor causing susceptibility to CAD in our population.


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