Associations between eNOS polymorphisms and susceptibility to systemic lupus erythematosus: a meta-analysis

Lee, Young Ho; Lee, Hye Soon; Choi, Sung Jae; Ji, Jong Dae; Song, Gwan Gyu

doi:10.1007/s00011-011-0397-3

Cited by 13 publications

(13 citation statements)

References 22 publications

(41 reference statements)

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“…Our findings contrast evidence found regarding other autoimmune diseases (26, 44–48). For example, in the Spanish population, no association was found between FCRL3 rs11264799 and MS (44).…”

Section: Discussioncontrasting

confidence: 99%

“…In the Chinese population, a significant association was not found between TNFAIP3 rs10499194 and SLE (45); however, carriers of the CT genotype and combined TT/CT genotype had an increased risk for RA in the Chinese Han population (46). A recent meta-analysis revealed that there was no association between TNFAIP3 rs10499194 and RA in Europeans, but a significant association in Asians (OR = 1.254, 95% CI = 1.101–1.429, p = 6.7 × 10 −4 ) (48). The discrepancies between our results and previous research may be attributed to differences in the populations and autoimmune diseases studied.…”

Section: Discussionmentioning

confidence: 99%

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Inflammation-Related Gene Polymorphisms Associated With Primary Immune Thrombocytopenia

Shao

et al. 2017

Front. Immunol.

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Primary immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by a reduced platelet count and an increased risk of bleeding. Although immense research has improved our understanding of ITP, the pathogenesis remains unclear. Here, we investigated the involvement of 25 single-nucleotide polymorphisms (SNPs) of the inflammation-related genes, including CD24, CD226, FCRL3, IL2, IRF5, ITGAM, NLRP3, CARD8, PTPN22, SH2B2, STAT4, TNFAIP3, and TRAF1, in the pathogenesis and treatment response of ITP. We recruited 312 ITP inpatients and 154 healthy participants in this case–control study. Inflammation-related SNP genotyping was performed on the Sequenom MassARRAY iPLEX platform. The expression of TNFAIP3 mRNA was determined by quantitative real-time RT-PCR. All SNPs in healthy controls were consistent with Hardy–Weinberg equilibrium. Statistical analysis revealed that rs10499194 in TNFAIP3 was significantly associated with a decreased risk of ITP after Bonferroni multiple correction (codominant, CT vs. CC, OR = 0.431, 95% CI = 0.262–0.711, p = 0.001; dominant, TT/CT vs. CC, OR = 0.249, 95% CI = 0.141–0.440, p = 0.000). Besides, TNFAIP3 expression was significantly higher in patients with CT and pooled CT/TT genotypes compared with CC genotype (p = 0.001; p = 0.001). Interestingly, rs10499194 was also associated with corticosteroid-sensitivity (codominant, CT vs. CC, OR = 0.092, 95% CI = 0.021–0.398, p = 0.001; dominant, TT/CT vs. CC, OR = 0.086, 95% CI = 0.020–0.369, p = 0.001; allelic, T vs. C, OR = 0.088, 95% CI = 0.021–0.372, p = 0.001). Furthermore, no significant association was found between inflammation-related SNPs and the severity or refractoriness of ITP after Bonferroni multiple correction. Our findings suggest that rs10499194 may be a protective factor for susceptibility and corticosteroid sensitivity in ITP patients.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inflammation-Related Gene Polymorphisms Associated With Primary Immune Thrombocytopenia

Shao

et al. 2017

Front. Immunol.

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“…Because of its relationship with inflammation, several studies have investigated the association of eNOS gene polymorphisms with inflammatory rheumatic diseases, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis and Behcet's disease (11,12,17,23,24). Some of these studies have yielded evidence of an association of the eNOS polymorphisms with either the pathogenesis of rheumatic diseases or extraarticular manifestations (12,17,23,24).…”

Section: Discussionmentioning

confidence: 99%

“…Some of these studies have yielded evidence of an association of the eNOS polymorphisms with either the pathogenesis of rheumatic diseases or extraarticular manifestations (12,17,23,24). It is well known that there is a strong genetic basis for AS, and some genes, particularly HLAB27, have already been implicated in disease pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…Based on these findings, we suggest that the NO pathway may be impaired and that this might be associated with genetic polymorphisms in the eNOS gene (2). Some reports have revealed an association between eNOS gene polymorphisms and inflammatory diseases (11,12,17,23,24). Because the pathogenesis of the genes is not fully understood in such inflammatory diseases, we wondered whether there was a link between eNOS gene polymorphisms and AS.…”

Section: Discussionmentioning

confidence: 99%

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Is there a relationship between endothelial nitric oxide synthase gene polymorphisms and ankylosing spondylitis?

Sarı¹,

İğci²,

Can³

et al. 2013

Clinics

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OBJECTIVE:Nitric oxide is produced by endothelial nitric oxide synthase, and its production can be influenced by polymorphisms of the endothelial nitric oxide synthase gene. Because candidate genes responsible for susceptibility to ankylosing spondylitis are mostly unknown and available data suggest that there may be problems related to the nitric oxide pathway, such as endothelial dysfunction and increased asymmetric dimethylarginine, this study aimed to assess the association of common endothelial nitric oxide synthase gene polymorphisms with ankylosing spondylitis.METHODS:One hundred ninety-four unrelated Turkish ankylosing spondylitis patients and 113 healthy without apparent cardiovascular disease, hypertension or diabetes mellitus were included. All individuals were genotyped by PCR-RFLP for two single-nucleotide polymorphisms, namely 786T>C (rs2070744, promoter region) and 786 Glu298Asp (rs1799983, exon 7). Variable numbers of tandem repeat polymorphisms in intron 4 were also studied and investigated by direct electrophoresis on agarose gel following polymerase chain reaction analysis. The Bath ankylosing spondylitis metrology index of the patients was calculated, and human leukocyte antigen B27 was studied.RESULTS:All studied polymorphisms satisfied Hardy-Weinberg equilibrium. Sex distributions were similar between the patient and control groups. No significant differences were found in the distributions of allele and genotype frequencies of the studied endothelial nitric oxide synthase polymorphisms between patients and controls. There were no correlations between endothelial nitric oxide synthase polymorphisms, disease duration, Bath ankylosing spondylitis metrology index or human leukocyte antigen B27.CONCLUSION:The results presented in this study do not support a major role of common endothelial nitric oxide synthase polymorphisms in Turkish ankylosing spondylitis patients.

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Brief Report: A Polymorphism in TLR2 Is Associated With Arterial Thrombosis in a Multiethnic Population of Patients With Systemic Lupus Erythematosus

Kaiser

Tang

Taylor

et al. 2014

Arthritis & Rheumatology

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ObjectiveThrombosis is a serious complication of systemic lupus erythematosus (SLE). Studies that have investigated the genetics of thrombosis in SLE are limited. We undertook this study to assess the association of previously implicated candidate genes, particularly Toll-like receptor (TLR) genes, with pathogenesis of thrombosis.MethodsWe genotyped 3,587 SLE patients from 3 multiethnic populations for 77 single-nucleotide polymorphisms (SNPs) in 10 genes, primarily in TLRs 2, 4, 7, and 9, and we also genotyped 64 ancestry-informative markers (AIMs). We first analyzed association with arterial and venous thrombosis in the combined population via logistic regression, adjusting for top principal components of the AIMs and other covariates. We also subjected an associated SNP, rs893629, to meta-analysis (after stratification by ethnicity and study population) to confirm the association and to test for study population or ethnicity effects.ResultsIn the combined analysis, the SNP rs893629 in the KIAA0922/TLR2 region was significantly associated with arterial thrombosis (logistic P = 6.4 × 10−5, false discovery rate P = 0.0044). Two additional SNPs in TLR2 were also suggestive: rs1816702 (logistic P = 0.002) and rs4235232 (logistic P = 0.009). In the meta-analysis by study population, the odds ratio (OR) for arterial thrombosis with rs893629 was 2.44 (95% confidence interval 1.58–3.76), without evidence for heterogeneity (P = 0.78). By ethnicity, the effect was most significant among African Americans (OR 2.42, P = 3.5 × 10−4) and European Americans (OR 3.47, P = 0.024).ConclusionTLR2 gene variation is associated with thrombosis in SLE, particularly among African Americans and European Americans. There was no evidence of association among Hispanics, and results in Asian Americans were limited due to insufficient sample size. These results may help elucidate the pathogenesis of this important clinical manifestation.

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Associations between eNOS polymorphisms and susceptibility to systemic lupus erythematosus: a meta-analysis

Abstract: This meta-analysis of published studies shows that the 4b/a polymorphism may be associated with the development of LN, and the C786T polymorphism may be associated with SLE susceptibility.

Cited by 13 publications

References 22 publications

Inflammation-Related Gene Polymorphisms Associated With Primary Immune Thrombocytopenia

Inflammation-Related Gene Polymorphisms Associated With Primary Immune Thrombocytopenia

Is there a relationship between endothelial nitric oxide synthase gene polymorphisms and ankylosing spondylitis?

Brief Report: A Polymorphism in TLR2 Is Associated With Arterial Thrombosis in a Multiethnic Population of Patients With Systemic Lupus Erythematosus

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