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Showing 2 results for Promoter

Soraya Larki, Dr Masoud Maleki,
Volume 6, Issue 1 (3-2018)
Abstract

Background and objectives: Endometrial tissue growth and its activity outside the uterus cause endometriosis. It has been suggested that various epigenetic deviations play a major role in the pathogenesis of endometriosis. Steroidogenic factor 1 (SF-1; NR5A1) is an essential transcription factor for estrogen biosynthesis in endometrial cells. The expression of SF-1 in endometriosis and lack of expression in normal endometrium is primarily determined by its promoter methylation. Here, we aimed to compare the methylation status of the SF-1 gene promoter region in women with endometriosis in comparison to healthy subjects.
Methods: In the present case–control study, DNA was extracted from 25 endometrial tissue samples from women with endometriosis and 5 normal post-hysterectomy endometrium tissues which were collected from Tabriz hospitals including Vali-e-Asr, Taleghani, 29 Bahman and Shams in 2016. The obtained DNA samples were subjected to Bisulfite-treatment. Finally, the status of SF-1gene promoter methylation was evaluated by methylation specific PCR method. Statistical analyses including descriptive and inferential statistics were conducted using tables, bar charts by statistical software SPSS version 20 and independence test.
Results: The methylation status of SF-1 gene promoter was decreased significantly in endometriosis samples (P<0.05).  
Conclusion: SF-1 gene promoter hypomethylation could increase the relative expression of SF-1 gene in endometriosis which may lead to the development or progression of the disease.
Golnesa Dadkhah, Hadi Bazzazi, Yaghoub Yazdani,
Volume 6, Issue 3 (9-2018)
Abstract

Background and objectives: Rheumatoid arthritis (RA) is a complex and systemic inflammatory disease in which the immune response is disturbed. Single nucleotide polymorphisms (SNPs) in the promoter regions of regulatory cytokines including interleukin-10 (IL-10) may lead to exacerbated immune response and increased risk of RA. Here, we aimed to assess the association of IL-10 -1082 (G/A) (rs1800896) promoter polymorphism with the susceptibility to RA in a population in northeast of Iran.
Methods: A total of 130 RA patients and 128 sex- and age- matched healthy donors were enrolled. The polymerase chain reaction (PCR) was used to amplify the polymorphic regions and restriction fragment length polymorphism (RFLP) technique was applied to detect rs1800896. SPSS 22.0 software was used to analyze data statistically.
Results: Our findings revealed that G allele was significantly associated with the increased risk of RA [OR = 1.88, 95% CI (1.32–2.66), P-value = 0.0001] in patients. Setting AA genotype as the reference, the AG [OR = 2.93, 95% CI (1.68–5.12), P-value = 0.0001] and GG [OR = 5.73, 95% CI (2.30–14.23), P-value = 0.0001] genotypes were significantly associated with RA susceptibility.
Conclusion: The present study suggests that the IL-10 -1082 (G/A) genetic variants are associated with RA susceptibility, but not with the disease activity. While this is the first time to report such an association in a population in northeast of Iran, further studies are needed to confirm these findings.

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