Ayşenur Ozderya

Istanbul University, İstanbul, Istanbul, Turkey

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Publications (6)13.15 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Graves' disease (GD) is a consequence of genetic and environmental factors. Endothelin 1 (EDN1) is a strong angiogenic and mitogenic factor, playing a key role in hypervascularization, thyroid follicule cell hyperplasia, and lymphocyte infiltration in the thyroid gland of patients with GD. EDN1 induces angiogenesis and mitogenesis via endothelin receptor type A (EDNRA). Relationships between their polymorphisms with several diseases have been found. This study examined the possible association of EDN1 (G5665T and T-1370G) and EDNRA (C+70G and G-231A) single nucleotide polymorphisms (SNPs) with the occurrence of GD, and evaluates the relationship between genotypes and clinical/laboratory manifestations of GD. We analyzed genotype and allele distributions of EDN1 and EDNRA polymorphisms in 165 patients with GD and 181 healthy controls by real-time PCR combined with melting curve analysis. No significant associations between GD and variant alleles of the studied polymorphisms were observed. However, the anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) levels in EDN1 G5665T GG genotype were higher than those in T allele carriers (GT+TT) (p=0.001 and p=0.026, respectively). In addition, anti-TPO levels in EDN1 T-1370G wild-type homozygous patients were found to be higher than in mutant gene carrying patients (GT+GG) (p=0.006). The presence of EDNRA+70G allele was associated with 3.37-fold increased risk for development of ophthalmopathy in GD patients (p=0.009). Although there were no associations between EDN1 (G5665T and T-1370G) and EDNRA (C+70G and G-231A) SNPs and susceptibility to GD, EDN1 G5665T and T-1370G polymorphisms were related to alterations of autoantibody production and EDNRA C+70G polymorphism is related with increased risk for ophthalmopathy in GD patients.
    International immunopharmacology 11/2013; · 2.21 Impact Factor
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    ABSTRACT: The etiopathogenesis of Graves' disease (GD) has not been clearly elucidated although the role of chronical inflammation and endothelial dysfunction has been established. Adhesion molecules such as intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), and E-selectin are secreted from vascular endothelium and promote accummulation of leukocytes in damaged endothelial areas. This study examined the possible association of ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) single nucleotide polymorphisms (SNPs) with the occurence of GD. ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs in DNA from peripheral blood leukocytes of 171 patients with GD and 259 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. We did not find significant differences in the distributions of studied polymorphisms, nor in the haplotype frequencies between patients with GD and healthy control. However, the anti-TPO levels in E-selectin 128R allele carrying subjects (SR + RR) were higher than S128S genotype (p < 0.05). In addition, the decline of TSH levels was more prominent in ICAM1 469 E carrying subjects (KE + EE) in comparison with wild homozygotes (p < 0.05). Although there is not assosiation between ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs and susceptibility to GD, higher anti-TPO in E-selectin 128 SR + RR, and lower TSH in ICAM1 469 KE + EE subjects suspect that these genotypes are prone to increased antithyroid autoantibody production with more accentuated TSH suppression in GD. Further studies with a larger cohort, analyzing other polymorphisms in ICAM, VCAM1 and E-selectin genes are necessary to support our observations.
    Molecular Biology Reports 12/2012; · 2.51 Impact Factor
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    ABSTRACT: This study examined firstly the possible association of G241R and K469E single nucleotide polymorphisms (SNPs) of ICAM-1 gene with the occurrence of Hashimoto thyroiditis (HT). G241R and K469E SNPs in DNA from peripheral blood leukocytes of 190 HT and 247 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. There was a significant increase of ICAM-1 241R allele frequency in patients with HT compared with healthy controls (P = 0.04, OR = 1.84, 95 % CI = 1.00-3.37). Regarding ICAM-1 K469E polymorphism, patients homozygous for E allele had 1.73-fold increased risk for developing HT according to KK homozygotes (P = 0.04, 95 % CI = 1.00-3.01). The 469E allele frequency was higher in HT patients according to controls, however the difference was at borderline significance (P = 0.05, OR = 1.30, 95 % CI = 1.00-1.70). No associations between polymorphisms and HT phenotypes were observed. We suggest that the G241R and K469E SNPs of ICAM-1 gene may be related to occurrence of HT. However, more studies with larger sample size including other loci of the ICAM-1 gene are necessary to support our findings before any definite statement can be made about the relationship between HT and ICAM-1 polymorphism.
    Molecular Biology Reports 10/2012; · 2.51 Impact Factor
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    ABSTRACT: BACKGROUND: Although prooxidant and antioxidant status were reported to be changed in clinical and experimental hypothyroidism, obtained results are conflicting. In addition, in subclinical hypothyroidism, scarced and controversial data are available about oxidative stress. Therefore, we aimed to investigate prooxidant-antioxidant status only in Hashimoto's thyroiditis (HT) patients with subclinical (sHT) and overt hypothyroidism (oHT). SUBJECTS AND METHODS: Thirty sHT and 18 oHT patients and 30 healthy control subjects were included in the study. Endogenous and prooxidant 2,2'-azobis-(2-amidinopropane) hydrochloride (AAPH)-induced malondialdehyde (MDA), diene conjugate (DC), protein carbonyl (PC) and nitrotyrosine (NT) levels as well as ferric reducing antioxidant power (FRAP) were determined in serum. In addition, endogenous DC and copper-induced MDA levels were measured in low density lipoprotein (LDL) fraction. RESULTS: Although there were no significant difference in serum endogenous MDA and DC levels, AAPH-induced MDA levels were significantly increased in sHT patients. All these parameters increased in oHT patients. Serum PC levels were detected to be increased in both sHT and oHT patients. Serum FRAP values did not alter in sHT patients, but they lowered in oHT patients. Endogenous DC and copper-induced MDA levels in LDL fraction did not change in sHT patients. However, these parameters were detected to be increased significantly in oHT patients as compared to controls and sHT patients. CONCLUSION: In conclusion, there were significant increases in oxidative stress parameters in serum and LDL-fraction in oHT patients. However, oxidative stress was detected to stimulate partly in serum, but not LDL fraction in sHT patients.
    International immunopharmacology 08/2012; 14(4):349-352. · 2.21 Impact Factor
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    ABSTRACT: Oxidative DNA damage, caused by either endogenous or exogenous sources of reactive oxygen species (ROS), has been linked several diseases including Graves' disease (GD). 7,8-Dihydro-8-oxoguanine (8-oxoG) is a major lesion produced by ROS and is considered a key biomarker of oxidative DNA damage. In humans, 8-oxoG is mainly repaired by 8-oxoguanine DNA N-glycosylase-1 (hOGG1), which is an essential component of the base excision repair (BER) pathway. The functional studies showed that hOGG1 Ser326Cys polymorphism is associated with the reduced DNA repair activity and increased risk for some oxidative stress-related diseases. In this study, we firstly investigated hOGG1 Ser326Cys polymorphism in GD. According to our results, Cys/Cys genotype frequency in the GD patients (23.4%) was significantly higher than the controls (9.2%). Cys/Cys genotype had an 3.5-fold [95% CI (confidence interval): 2.10-6.01, p < 0.001] the Cys allele had 1.83-fold (95% CI: 1.43-2.34, p < 0.001) increase in the risk for developing GD. Our results suggest that Ser326Cys polymorphism of the hOGG1 gene is associated with GD risk.
    Cell Biochemistry and Function 04/2011; 29(3):244-8. · 1.85 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: Oxidative stress has been implicated in etiopathogenesis of Graves' disease (GD). Increased lipid peroxidation and oxidative DNA damage have been found in GD patients. Oxidative DNA damage is mainly repaired by the base-excision repair (BER) pathway. Polymorphisms in DNA-repair genes have been associated with the increased risk of various diseases and could also be related to the etiology of GD. Therefore, we conducted a study including 197 patients with GD and age- and sex-matched 303 healthy subjects to examine the role of single-nucleotide polymorphisms of BER genes, APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) as a risk factor for GD. These polymorphisms were determined by quantitative real-time PCR and melting curve analysis using LightCycler. No significant association was observed between the variant alleles of APE/Ref-1 codon 148 [odds ratio (OR) = 0.89, 95% confidence interval (CI) = 0.69-1.17], XRCC1 codon 194 (OR = 1.24, 95% CI = 0.79-1.94), and XRCC1 codon 399 (OR = 1.12, 95% CI = 0.86-1.46) and GD. These preliminary results suggest that APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) polymorphisms are not significant risk factors for developing GD.
    Cell Biochemistry and Function 09/2009; 27(7):462-7. · 1.85 Impact Factor

Publication Stats

5 Citations
401 Views
13.15 Total Impact Points

Institutions

  • 2009–2013
    • Istanbul University
      • • Department of Medical Biochemistry
      • • Department of Family Medicine (Istanbul Medical Faculty)
      İstanbul, Istanbul, Turkey
  • 2012
    • Sisli Etfal Training and Research Hospital
      İstanbul, Istanbul, Turkey