Association of Tumor Necrosis Factor Alpha-Induced Protein 3 Interacting Protein 1 (TNIP1) Gene Polymorphism (rs7708392) with Lupus Nephritis in Egyptian Patients

Rizk, Mohamed M.; Tayae, Eman; Elkeraie, Ahmed; Ramzy, Ireny

doi:10.1007/s10528-018-9855-8

Cited by 12 publications

(11 citation statements)

References 37 publications

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“…The most reported TNIP1 variant associated with SLE and LN is rs7708392. This SNP has been replicated in several different SLE cohorts including European and Chinese, 16 17 North American, 18 Egyptian, 19 Japanese, 20 Swedish 21 and Hispanic 22 populations. Our group found a strong association for rs7708392 with LN in European Americans (EA) in a large-scale study of North American patients with SLE.…”

Section: Introductionmentioning

confidence: 80%

“… 20 A study of a Egyptian cohort that included 53 SLE patients with LN, 57 SLE patients without nephritis and 85 healthy controls showed that rs7708392 was significantly more prevalent among patients with LN than in patients without LN. 19 However, there are discrepancies as to which allele of rs7708392 is associated with increased risk. Our group identified the minor C allele to be associated with increased risk for LN in North American patients with SLE with European ancestry.…”

Section: Introductionmentioning

confidence: 99%

“… 20 Conversely, Rizk et al determined that Egyptian patients with SLE had a 3.4-fold increase in risk of developing LN if they contained one G allele. 19 Subsequently, Zhong et al found the G allele to be protective in the Chinese population, but given its low frequency in Asian populations (30%) compared with European populations (70%) they suggest there is genetic heterogeneity in this locus between different populations, which may explain the observed discrepancies. 17 …”

Section: Introductionmentioning

confidence: 99%

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TNIP1/ABIN1 and lupus nephritis: review

Brady

Korte²,

Caster

et al. 2020

Lupus Sci Med

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SLE is a complex autoimmune disease with genetic, epigenetic, immune-regulatory, environmental and hormonal factors. Kidney inflammation and injury, termed lupus nephritis (LN), occurs in over half of patients with SLE and is a leading cause of disability and death. There is a high degree of short-term and long-term side effects associated with current LN therapies and they are not effective for many patients. Thus, novel therapies with reduced toxicity and improved efficacy are drastically needed. Many of the known LN susceptibility genes have functions that mediate inflammation via cytokine/chemokine production and activation of myeloid and B cells. Understanding the cellular and molecular mechanisms mediated by these variant gene products provides valuable insight for the development of improved and personalised diagnostics and therapeutics. This review describes variants in the TNIP1 (tumour necrosis factor α-induced protein 3-interacting protein 1) gene associated with risks for SLE and LN and potential roles for loss of function of its protein product ABIN1 in the activation of myeloid and B-cell-mediated injury in LN.

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Section: Introductionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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TNIP1/ABIN1 and lupus nephritis: review

Brady

Korte²,

Caster

et al. 2020

Lupus Sci Med

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“…The relations among polymorphisms of several inflammatory regulatory genes, such as STAT4 , TNF‐α‐Induced Protein 3 Interacting Protein 1 ( TNIP1 ), Interferon regulatory factor 5 ( IRF5 ), interleukin‐10 promoter, TNF‐α Promoter and SLE were conducted. We evaluated the effect of COX‐2 rs2745557 gene polymorphism on SLE.…”

Section: Discussionmentioning

confidence: 99%

Association between COX‐2 and 15‐PGDH polymorphisms and SLE susceptibility

et al. 2020

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Int J Rheum Dis. 2020;23:627-632. | 627 wileyonlinelibrary.com/journal/apl | INTRODUC TI ONSystemic lupus erythematosus (SLE) is a heterogeneous and chronic inflammatory autoimmune disease which has important features, such as autoantibody production against host nuclear antigens and multi-organ inflammation (like skin, kidneys, and brain). 1,2 Its occurrence is more common in women than men. 3 SLE etiology is unknown. Environmental factors, such as UV radiation, AbstractAims: Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease. Prostaglandins E2 (PGE2), the product of the cyclo-oxygenase 2 (COX-2) enzyme, has critical roles in the etiology of autoimmune diseases. PGE2 level is controlled by a balance between its synthesis mediator (COX-2 enzyme) and its catabolic key enzyme (15-hydroxyprostaglandin dehydrogenase [15-PGDH] enzyme). In the present study, the associations of genotypic polymorphisms in COX-2 and 15-PGDH with SLE were investigated. Methods: One hundred and sixty SLE patients and 160 healthy controls participated in the study. The polymerase chain reaction -restriction fragments length polymorphism method was used for genotyping. The COX-2 rs2745557 G/A and 15-PGDH rs8752 G/A polymorphisms were investigated. Results:Regarding the COX-2 rs2745557 single nucleotide polymorphism, there was no significant association between COX-2 rs2745557 polymorphism and SLE.However, the dominant models showed a marginally significant relation (P = .048, odds ratio = 0.63, 95% CI = 0.4-1.0). Regarding GA genotype of 15-PGDH rd8752 polymorphism, there was a significant difference between two groups with a 4.5-fold increase in SLE development (P = .0001). The frequency of the A allele was higher in SLE patients than that in controls, showing a 1.4-fold increase in SLE development (P = .018). Conclusion:All results showed the protective effects of the dominant model of COX-2 rs2745557 polymorphism and risk factor of 15-PGDH rs8752 polymorphism on SLE development. K E Y W O R D S15-PGDH, COX-2, polymorphism, systemic lupus erythematosus Photosensitivity, n (%) 79 (49.4) Discoid rash, n (%) 6 (3.8) Mouth ulcers, n (%) 38 (23.8) Hair loss, n (%) 42 (26.3) Arthritis, n (%) 116 (72.5) Leukopenia, n (%) 30 (18.8) Thrombocytopenia, n (%) 35 (21.9) Renal disease, n (%) 21 (13.1) Antiphospholipid syndrome, n (%) 7 (4.4) Anti-double-stranded DNA, n (%) 108 (67.5) Antinuclear antibodies, n (%) 111 (69.4) Abbreviation: SLE, systemic lupus erythematosus. How to cite this article: Sandoughi M, Saravani M, Rokni M, Nora M, Mehrabani M, Dehghan A. Association between COX-2 and 15-PGDH polymorphisms and SLE susceptibility. Int J Rheum Dis. 2020;23:627-632. https ://doi.

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“…The TNIP1 rs3792783 SNP, located in an intronic region, has been previously associated with antibody-positive primary Sjögren’s syndrome [36] and systemic sclerosis [40], and seems to be a risk factor for Vogt–Koyanagi–Harada syndrome [41]. Also, the TNIP1 rs7708392 SNP, also located in an intronic region of TNIP1, has been related to a higher risk of developing lupus nephritis [42,43], lupus erythematosus [44,45,46], autoimmune hepatitis [47], and Sjögren’s syndrome [36]. Among septic patients, this is the first study investigating the role of TNIP1 SNPs on this disease.…”

Section: Discussionmentioning

confidence: 99%

TNFAIP3, TNIP1, and MyD88 Polymorphisms Predict Septic-Shock-Related Death in Patients Who Underwent Major Surgery

Jiménez-Sousa

Fuentes

Liu

et al. 2019

JCM

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Background: In many immune-related diseases, inflammatory responses and several clinical outcomes are related to increased NF-κB activity. We aimed to evaluate whether SNPs related to the NF-κB signaling pathway are associated with higher susceptibility to infection, septic shock, and septic-shock-related death in European patients who underwent major surgery. Methods: We performed a case-control study on 184 patients with septic shock and 212 with systemic inflammatory response syndrome, and a longitudinal substudy on septic shock patients. Thirty-three SNPs within genes belonging to or regulating the NF-κB signaling pathway were genotyped by Agena Bioscience’s MassARRAY platform. Results: No significant results were found for susceptibility to infection and septic shock in the multivariate analysis after adjusting for multiple comparisons. Regarding septic-shock-related death, patients with TNFAIP3 rs6920220 AA, TNIP1 rs73272842 AA, TNIP1 rs3792783 GG, and TNIP1 rs7708392 CC genotypes had the highest risk of septic-shock-related death in the first 28 and 90 days. Also, the MyD88 rs7744 GG genotype was associated with a higher risk of death during the first 90 days. Haplotype analysis shows us that patients with the TNIP1 GAG haplotype (composed of rs73272842, rs3792783, and rs7708392) had a lower risk of death in the first 28 days and the TNIP1 AGC haplotype was associated with a higher risk of death in the first 90 days. Conclusions: The SNPs in the genes TNFAIP3, TNIP1, and MyD88 were linked to the risk of septic-shock-related death in patients who underwent major surgery.

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Association of Tumor Necrosis Factor Alpha-Induced Protein 3 Interacting Protein 1 (TNIP1) Gene Polymorphism (rs7708392) with Lupus Nephritis in Egyptian Patients

Cited by 12 publications

References 37 publications

TNIP1/ABIN1 and lupus nephritis: review

TNIP1/ABIN1 and lupus nephritis: review

Association between COX‐2 and 15‐PGDH polymorphisms and SLE susceptibility

TNFAIP3, TNIP1, and MyD88 Polymorphisms Predict Septic-Shock-Related Death in Patients Who Underwent Major Surgery

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