Polymorphism of the NFKB1 affects the serum inflammatory levels of IL-6 in Hashimoto thyroiditis in a Turkish population

Koc, Arzuhan; Batar, Bahadır; Çelik, Özlem; Onaran, İlhan; Taşan, Ertuğrul; Sultuybek, Gönül Kanıgür

doi:10.1016/j.imbio.2014.03.009

Cited by 29 publications

(22 citation statements)

References 40 publications

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“…Romozova et al [29] investigated the A/G point variation in the 3’UTR region of NFKBIA gene in Czech and German cases with type 2 diabetes, demonstrated that AA genotype of 3’UTR A/G variant is associated with diabetes risk. Koc et al [30] investigated the relationship between 3’UTR A/G polymorphism and NFKB1-94ins/del ATTG polymorphism, and the risk of Hashimoto thyroiditis in a Turkish Population, concluded that ins/ins/GG combined genotype had protective effect on the disease and this protectiveness was based on G allele of NFKBIA3’UTR A/G polymorphism. To the best of our knowledge, there have been no reports on the effects of 3’UTR A/G polymorphism of NFKBIA on CAD risk in Chinese population.…”

Section: Discussionmentioning

confidence: 99%

Genetic Variation in NFKB1 and NFKBIA and Susceptibility to Coronary Artery Disease in a Chinese Uygur Population

Lai

Yang

et al. 2015

PLoS ONE

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ObjectivesCoronary artery disease (CAD) is the most common chronic inflammatory disease worldwide. NF-κB, a central regulator of inflammation, is involved in various inflammatory diseases. The aim of this study was to investigate the association between NFKB1 and NFKBIA polymorphisms and the susceptibility to CAD and their impact on plasma levels of IL-6 in a Chinese Uygur population.MethodsWe genotyped NFKB1-94ins/del ATTG (rs28362491) and NFKBIA3’ UTR A/G (rs696) using TaqMan SNP genotyping assays in 960 Uygur CAD cases and Uygur 1060 CAD-negtive controls. IL-6 plasma levels were measured in 360 stable angina pectoris (SAP) cases and 360 controls using ELISA method.ResultsThere was no significant difference in the distribution of the genotypes and alleles of rs696 polymorphism in CAD cases and controls. Significant difference in the frequency of genotypes (P = 0.001) and alleles (P = 0.001) of rs28362491 polymorphism was observed in CAD cases compared to controls. In multivariate logistic regression analysis, SNP rs28362491 was consistently associated with CAD risk in a recessive model after adjustment for cardiovascular risk factors (OR = 1.581, 95% CI 1.222 to 2.046, P<0.001). SAP cases had significantly higher plasma levels of IL-6 compared to controls (P<0.001). General linear model analysis showed rs28362491 was independently associated with increased IL-6 levels by analyses of a recessive model (P<0.001) after adjustment for covariates.ConclusionsOur study indicates that NFKB1-94 ins/del ATTG polymorphism may play a role in CAD susceptibility in Chinese Uygur population and is functionally associated with IL-6 expression, suggesting a mechanistic link between NFKB1-94 ins/del ATTG polymorphism and CAD susceptibility.

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Section: Discussionmentioning

confidence: 99%

Genetic Variation in NFKB1 and NFKBIA and Susceptibility to Coronary Artery Disease in a Chinese Uygur Population

Lai

Yang

et al. 2015

PLoS ONE

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“…One of the most prominent polymorphisms known within the promoter of this gene is -94 ins/del ATTG rs28362491. A potential candidate for searching pathogenesis of inflammatory diseases, rs28362491, is shown to be associated with increased risk in rheumatoid arthritis [24], Graves's disease [25] and type 1 diabetes mellitus [26], whereas no associations with Hashimoto thyroiditis (HT) [27] and multiple sclerosis [28] have been yet shown. In addition, in American [13] and Dutch populations [29], rs28362491 in the NFKB1 gene was associated with UC development but not in Spanish [30] and British populations [31].…”

Section: Discussionmentioning

confidence: 99%

Association of NFKB1 and NFKBIA Polymorphisms in Relation to Susceptibility of Behçet's Disease

et al. 2014

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Behc ßet's disease (BD) is a chronic inflammatory autoimmune disease. Although raised levels of proinflammatory cytokines in BD have been reported, the pathogenesis is still unknown. The aim of this study was to investigate the association of NFKB1 and NFKBIA polymorphisms and their single and combined analysis effects on susceptibility of BD in Turkish population. We analysed the distribution of NFKB1 -94 ins/del ATTG (rs28362491) and NFKBIA 3 0 UTR A?G (rs696) polymorphisms using PCR-RFLP method in 89 patients with BD and 190 controls in this population. Statistical analysis of the results was performed by calculating OR, and 95% CI via v 2 test and using Bonferroni correction. According to the significant results of both single and combined genotype analysis, the frequencies of ins/ins genotype and ins allele of rs28362491 were significantly higher in patients with BD (Pc = 0.003, 0.004, respectively). Also, higher frequencies of the rs696 variant containing AA genotype was found in patients with BD (Pc = 0.0033), whereas no statistical significant differences in distribution of the alleles of rs696 polymorphism in patients and controls. In addition, according to the combined genotype analysis, the wild type of both rs28362491 and rs696 polymorphisms (ins/ins/AA genotype) was also significantly higher in BD cases (Pc = 0.044). Our findings prove that both single and combined genotype analysis of rs28362491 and rs696 polymorphisms indicate that the wild genotypes of both two SNPs (ins/ins and AA genotypes) and ins/ins/AA combined genotype are strongly associated with enhanced risk of BD in a Turkish population.

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“…Patients and controls were genotyped for the miR - 146a - 3p (rs2910164, G > C) alleles using a polymerase chain reaction (PCR) amplification employing the LightSNiP assay (TIB MOLBIOL, Berlin, Germany). Capillary electrophoresis or PCR followed by restriction fragment length polymorphism (PCR–RFLP with Pfl Ml digestion) were employed to study the NFkB1 (rs28362491, ins/del ATTG) alleles, as previously described by Zhou et al (2009) and Koc et al (2014), respectively. Separation of PCR products was performed in a 50 cm 8 capillary array containing POP-7 polymer on 3500 Genetic Analyzer (Applied Biosystem, USA) and analyzed by GeneMapper Software v 4.2 (Applied Biosystem, USA).…”

Section: Methodsmentioning

confidence: 99%

Significance of Polymorphism and Expression of miR-146a and NFkB1 Genetic Variants in Patients with Rheumatoid Arthritis

Bogunia‐Kubik

Wysoczańska

Piątek

et al. 2016

Arch. Immunol. Ther. Exp.

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MicroRNA-146a (miR-146a) has been shown to play an important role in the regulation of inflammatory innate immune responses, and found to be differentially expressed in rheumatoid arthritis (RA). Through NF-κB pathway, this molecule is able to stimulate the release of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-17. It has been also suggested that single-nucleotide polymorphisms (SNPs) in miRNA sequences may alter miRNA expression and that miR-146a rs2910164 SNP may contribute to RA development. These observations prompted us to analyze the potential associations between the miR-146a-3p (rs2910164, G > C) and NFkB1 (rs28362491, ins/del ATTG) polymorphisms and miR-146a-5p expression in patients’ sera in relation to clinical outcome of the treatment as well as predisposition to RA. Genotyping was performed in 111 patients and 130 healthy individuals while 16 controls and 13 RA patients (before and after three months of therapy with TNF-α inhibitors (TNFi)) were studied for the circulating miR-146a-5p serum expression level. Patients carrying the NFkB1 ins/ins genotype were characterized by worse response to TNFi treatment (p = 0.023). In patients, before TNFi therapy, expression levels of miR-146a-5p were less (0.422 ± 0.171) as compared to those detected after three months of treatment (1.809 ± 0.658, p = 0.033) and observed for healthy controls (5.302 ± 2.112, p = 0.048). Moreover, patients with higher circulating miR-146a-5p levels after three months of TNFi administration were more frequently carrying the rs2910164-C allele (p = 0.032). These results support the hypothesis that miR-146a might be involved in pathogenesis of RA and imply that miR-146a-3p polymorphism may be associated with miR-146a-5p levels in serum after anti-TNF-α treatment.

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Polymorphism of the NFKB1 affects the serum inflammatory levels of IL-6 in Hashimoto thyroiditis in a Turkish population

Cited by 29 publications

References 40 publications

Genetic Variation in NFKB1 and NFKBIA and Susceptibility to Coronary Artery Disease in a Chinese Uygur Population

Genetic Variation in NFKB1 and NFKBIA and Susceptibility to Coronary Artery Disease in a Chinese Uygur Population

Association of NFKB1 and NFKBIA Polymorphisms in Relation to Susceptibility of Behçet's Disease

Significance of Polymorphism and Expression of miR-146a and NFkB1 Genetic Variants in Patients with Rheumatoid Arthritis

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