Browsing by Author "Ozdas, Sibel"

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Association of Interleukin-10 Gene Promoter Polymorphisms with Obstructive Sleep Apnea
(2016) Ozdas, Sibel; Ozdas, Talih; Acar, Mustafa; Erbek, Selim S.; Koseoglu, Sabri; Gokturk, Gokhan; Izbirak, Afife; https://orcid.org/0000-0003-4825-3499; 26139223; B-7604-2019
Interleukin-10 (IL) is an anti-inflammatory cytokine that regulates normal sleep patterns, and recent studies have reported that it is a potential useful biomarker to identify presence and severity of sleep apnea syndrome (OSAS). Promoter polymorphisms of IL-10 gene have been associated with altered expression levels, which contributes to OSAS. The aim of this study was to determine the prevalence of -1082 G/A, -819 C/T, and -592 C/A promoter polymorphisms of IL-10 gene in individuals with OSAS and controls. An open-label study was performed in the Otorhinolaryngology and Sleep Disorders Outpatient Clinics. One hundred four cases with OSAS were included as the study group, and 78 individuals without OSAS were included as the controls. DNAs were extracted from peripheral blood leukocytes, and the sites that encompassed those polymorphisms were identified by DNA sequencing analyses. Data were analyzed with SNPStats and multifactor dimensionality reduction (MDR) software. The prevalence of OSAS was higher in males in the study group when compared to controls (P = 0.0003). The IL-10-1082 G/A, -819 C/T, and -592 C/A SNPs, and their minor alleles were associated with a significantly increased risk for OSAS compared to the controls (P E, 0.05 for all). Furthermore, ATA haplotype frequency was significantly higher in the study group compared to the control group, but the GCC haplotype frequency was lower (P = 0.0001 and P = 0.0001). As indicated in MDR analysis, combinations of IL-10 gene were associated with OSAS in single-, double-, and triple-locus analyses. The prevalences of the IL-10 gene promoter polymorphisms were different in OSAS patients and the controls in Turkish population. IL-10 gene polymorphisms may lead to altered inflammatory cascade, which might contribute to OSAS. Further studies on larger cohorts are needed to validate our findings.
Investigation of SCGB3A1 (UGRP2) Gene Arrays in Patients with Nasal Polyposis
(2014) Palali, Mehmet; Ozcan, K. Murat; Ozdas, Sibel; Koseoglu, Sabri; Ozdas, Talih; Erbek, Selim S.; Yildirim, Erol; Ensari, Serdar; Dere, Huseyin; https://orcid.org/0000-0003-4825-3499; 24710847; B-7604-2019
The aim of the current study is to investigate the potential relationship between polymorphisms and nasal polyposis (NP) pathogenesis in the SCGB3A1 (UGRP2) gene, which is a member of the secretoglobin gene super family. Genotypic variations were studied by performing DNA sequencing in blood samples of 80 patients with NP and 70 healthy individuals to evaluate nucleotide changes and their positions that might be in the SCGB3A1 gene (promotor, splicing points, and exon distributions). In the SCGB3A1 gene, three single-nucleotide changes labeled IVS1-89 T > G, c. -183 G > T, IVS1-189 G > A were identified. IVS1-89 T > G and IVS1-189 G > A belong to the first intronic region of the gene, whereas c. -183 G > T was observed in the promoter region of the gene. The IVS1-89 T > G nucleotide change was observed in the patient and control groups, whereas c. -183 G > T and IVS1-189 G > A nucleotide changes were observed in the control group only. SCGB3A1 (IVS1-89) genotype frequencies between patients with NP and control group were not significantly different (p = 0.311). There was a statistically significant difference in the control group in comparison to patients with NP in terms of SCGB3A1 (c. -183 GT) and SCGB3A1 (IVS1-189 GA) frequency (p = 0.0045 and p = 0.009, respectively). The findings of the current study suggest that SCGB3A1-183 T and SCGB3A1 IVS1-189 A alleles might have a protective effect against NP, and that SCGB3A1 (-183 GT and IVS1-189 GA) genotypes should be studied in future population-based studies.
Role of Single Nucleotide Polymorphisms of Mammaglobin-A Gene in Nasal Polyposis: A Case Control Study
(2020) Oz, Isilay; Ozdas, Sibel; Bastimur, Sibel; Ozdas, Talih; Muz, Sami Engin; Atilla, Huntuk; Kurt, Kenan; Erbek, Selim; 0000-0003-4825-3499; 0000-0002-7380-4566; B-7604-2019; AAJ-1452-2021
Objective: Nasal Polyposis (NP) is a chronic inflammatory disease and genetic factors play an important role in the pathophysiology. Mammaglobin-A (MGA) gene expression was significantly higher in patients with NP and chronic rhinosinusitis compared to normal mucosa. In the present study, we investigated the relationship between single nucleotide polymorphisms (SNPs) in the MGA gene and nasal polyposis in the Turkish population. Materials and Methods: A total of 87 patients diagnosed with NP and 60 healthy volunteers were enrolled in the study. Genotypes of MGA promoter SNPs c38C>G, c.21C>T, c55+186G>A and c.243+230A>T were determined by light SNP ASSAY after real time PCR analysis using genomic DNA samples obtained from the peripheral blood samples of all participants. Results: A total of 87 NP patients, 51 male and 36 female, with a mean age of 38.18 +/- 9.5 years were included in the study. No significant difference was determined at all positions c38C>G, c.21C>T, c55+186G>A and c.243+230A>T in nasal polyp patients compared to controls with and without allergic rhinitis (AR). Conclusion: MGA gene c38C>G, c.21C>T, c55 + 186G>A, and c.243 + 230A>T genotypes did not appear to be associated with susceptibility to NP with and without AR in our study population.
Single-Nucleotide Polymorphisms on the RYD5 Gene in Nasal Polyposis
(2015) Ozdas, Sibel; Izbirak, Afife; Ozdas, Talih; Ozcan, Kursat Murat; Erbek, Selim S.; Koseoglu, Sabri; Dere, Huseyin; 26204469
Nasal polyposis (NP) is a chronic inflammatory disease. Several genes play major roles in the pathophysiology of the disease. We analyzed RYD5 gene polymorphisms to determine the effect of these variants or their genetic combinations on NP. We genotyped the RYD5 gene in 434 participants (196 patients with NP and 238 controls). Data were analyzed with SPSS, SNPStats, and multifactor dimensionality reduction (MDR) software. We genotyped 10 single-nucleotide polymorphisms (SNPs) in the RYD5 gene. RYD5 (+152G>T) (p.Gly51Va) has not been reported previously. The PolyPhen and PROVEAN predicted the missense mutation as deleterious, but sorting intolerant from tolerant (SIFT) did not. In the genotype analysis, we found that four SNPs (RYD5 [-264A>G], [-103G>A], [+57-14C>T], and [+66A>G]) were significantly associated with NP. The individuals with combined genotypes of six risk alleles (RYD5-264G, -103A, +13C, +57-14T, +66G, and +279T) had significantly higher risks for NP compared with the ones with one or four risk alleles. Haplotype analysis revealed that the two haplotypes were associated with risk of NP. As indicated by MDR analysis, RYD5 (-264A>G and -103G>A) and RYD5 (-264A>G, -177C>A, and -103G>A) were the best predictive combinations and they had the highest synergistic interaction on NP. In addition, RYD5 (+13C>T) was significantly associated with increased risk of both NP with asthma and NP with allergy and asthma. Some SNPs and their combinations in the RYD5 gene are associated with increased probability for developing NP. We emphasize the importance of genetic factors on NP and NP-related clinical phenotypes.