Association of Tumor Necrosis Factor (TNF) promoter polymorphisms with plasma TNF-α levels and susceptibility to diabetic nephropathy in North Indian population

Gupta, Stuti; Mehndiratta, Mohit; Kalra, Sarathi; Kalra, Om Prakash; Shukla, Rimi; Gambhir, Jasvinder K.

doi:10.1016/j.jdiacomp.2015.01.002

Cited by 21 publications

(32 citation statements)

References 33 publications

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“…−1031T/C polymorphism is located in the regulatory region of TNF‐ α gene and there is some evidence that it may also affect TNF‐α production. For example, a study in diabetes disease found that T allele of −1031T/C polymorphism was associated with lower plasma TNF‐α level (Gupta et al, ). Our previous finding demonstrated that serum levels of TNF‐α were significantly decreased in the schizophrenia patients compared with control subjects (Lv et al, ).…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor‐alpha −1031T/C polymorphism is associated with cognitive deficits in chronic schizophrenia patients versus healthy controls

Xiu

Man

Wang

et al. 2018

American J of Med Genetics Pt B

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Recent compelling research has demonstrated a pathophysiologic role for proinflammatory cytokines of microglial origin in decreasing neurocognitive function. Psychiatric diseases are already known to have reduced cognitive function and are also associated with increased inflammation. To elaborate on these data, our study aims to investigate how a particular polymorphism of the tumor necrosis factor gene, TNF-α -1031T/C, affects neurocognitive performance in patients with schizophrenia. We recruited 905 patients with schizophrenia and 571 healthy control subjects. We employed the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) to test for neurocognitive function and the positive and negative syndrome scale to evaluate schizophrenia severity. The -1031T/C polymorphism was genotyped in both healthy controls and schizophrenic patients. Our results demonstrate that patients with the C allele (either T/C or C/C) possessed increased immediate memory index, visuospatial/constructional index, and RBANS total scores as compared to patients without it (p < .05). In healthy controls, there was no significant difference across genotypes (p > .05). Our findings demonstrate that the TNF-α -1031T/C polymorphism may not play a role in the susceptibility of schizophrenia itself, but may be involved in the cognitive deficits of schizophrenia. This suggests an important role for cytokine signaling in mediating the severity of cognitive dysfunction in schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor‐alpha −1031T/C polymorphism is associated with cognitive deficits in chronic schizophrenia patients versus healthy controls

Xiu

Man

Wang

et al. 2018

American J of Med Genetics Pt B

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“…In addition, previous studies have produced related evidence [7,11,18]. Consistent with rs2794521 and rs1800796, the exchange of T to C allele at -1031 locus in the TNF gene was associated with T2DM [12][13]. Nevertheless, study outcomes regarding the relationship between selected genetic polymorphisms and T2DM risk are in disagreement.…”

Section: Introductionmentioning

confidence: 81%

“…Genetic variants of in ammation-related genes are believed to play roles in the development of elevated blood glucose, due to their ability to modulate concentrations of in ammatory cytokines [9,[11][12] which may consequently affect the glucose pathway and eventually result in T2DM [2][3]. In this study, we investigated whether polymorphisms rs2794521 of the CRP gene, rs1800796 of the IL6 gene and rs1799964 of the TNF gene are related to elevated blood glucose among the Thai population.…”

Section: Discussionmentioning

confidence: 99%

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A transition of C to G (rs1800796) at promoter region of IL6 gene is associated with lowered risk of elevated blood glucose in rural Thais

Phosat

Phienluphon

Hananantachai

et al. 2019

Preprint

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Background Inflammation has been associated with increased risk of type 2 diabetes mellitus (T2DM). Thus, polymorphisms of genes encoding pro-inflammatory cytokines may influence the condition. This study aimed to determine the association between genetic variations in inflammation-related genes, including rs2794521 of the CRP gene, rs1800796 of the IL6 gene, and rs1799964 of the TNF gene, and risk of elevated blood glucose.Methods A total of 296 subjects were allocated to either the control group (n=135) or elevated blood glucose group (n=161). The studied single nucleotide polymorphisms were investigated among 296 subjects by real-time PCR technique. Logistic regression model was used to evaluate the association between the genetic variations and risk of elevated blood glucose.Results Both dietary intake and concentrations of inflammatory cytokines (CRP, IL6, and TNF-α) in the subjects with different genotypes were analogous. AG carriers of rs2794521 CRP showed the highest levels of obesity indices (BMI, waist circumference, and body fat; p<0.05 for all) compared to wild type. Homozygous variants of rs1800796 (GG) and rs1799964 (CC) were associated with significantly lower HbA1c level ( p =0.041) and fasting blood glucose concentration ( p =0.043), respectively. An association with decreased risk of elevated blood glucose was found among GG female carriers of rs1800796 [OR 0.23 (0.06-0.87), p =0.031]. A tendency towards lowered blood glucose was also seen in AGT carriers [OR 0.49 (0.024-1.02), p =0.058).Conclusions The polymorphisms rs2794521 CRP, rs1800796 IL6, and rs1799964 TNF were associated with risk of T2DM. Individuals who carried GG of rs1800796 or -717A-572G-1031T displayed a lower risk of T2DM.

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“…recognized to serve a crucial function in the pathogenesis and clinical outcome of DN (36,37). However, therapeutic strategies targeting cytokine promotion are effective against DN.…”

Section: A B C Dmentioning

confidence: 99%

SOCS3 overexpression inhibits advanced glycation end product-induced EMT in proximal tubule epithelial cells

Lin

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Diabetic nephropathy (DN) is among the most severe complications of diabetes mellitus, and may lead to end-stage renal disease. Sustained exposure to advanced glycation end products (AGEs) typically causes renal tubular epithelial cells (TECs) to suffer from an epithelial-to-mesenchymal transition (EMT). However, there remains no consensus regarding the mechanism underlying the cause of EMT in TECs as induced by AGEs. In the present study, we investigated the promotion of EMT in TECs by AGEs, and the activation of Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling. In addition, we constructed a recombinant adenovirus (Ad) that overexpressed suppressor of cytokine signaling 3 (SOCS3), and examined the regulatory role of SOCS3 in the activation of JAK/STAT signaling and the promotion of EMT in TECs. The results demonstrated that AGE-bovine serum albumin (BSA) treatment significantly promoted the expression of EMT-associated proteins, while reducing the expression of the epithelial cell marker, E-cadherin. Furthermore, the Ad-mediated SOCS3 overexpression markedly inhibited the AGE-BSA-induced JAK2/STAT3 activation; phosphorylated JAK2 and phosphorylated STAT3 expression levels were reduced by the Ad-SOCS3 infection, compared with the control Ad (Ad-con) infection, in HK-2 cells subject to AGE-BSA. Moreover, the overexpression of SOCS3 markedly inhibited the AGE-BSA-promoted EMT in HK-2 cells. AGE-BSA-promoted EMT-associated proteins, such as α-smooth muscle actin and collagen I, were reduced by the Ad-SOCS3 virus infection, in contrast to the Ad-con virus infection. Furthermore, reduced E-cadherin expression was reversed by the Ad-SOCS3 virus infection, in contrast to the Ad-con virus infection, in epithelial HK-2 cells. In conclusion, the present study confirmed the inhibitory role of SOCS3 in the AGE-induced EMT in renal TECs, implying the protective role of SOCS3 in DN.

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Association of Tumor Necrosis Factor (TNF) promoter polymorphisms with plasma TNF-α levels and susceptibility to diabetic nephropathy in North Indian population

Cited by 21 publications

References 33 publications

Tumor necrosis factor‐alpha −1031T/C polymorphism is associated with cognitive deficits in chronic schizophrenia patients versus healthy controls

Tumor necrosis factor‐alpha −1031T/C polymorphism is associated with cognitive deficits in chronic schizophrenia patients versus healthy controls

A transition of C to G (rs1800796) at promoter region of IL6 gene is associated with lowered risk of elevated blood glucose in rural Thais

SOCS3 overexpression inhibits advanced glycation end product-induced EMT in proximal tubule epithelial cells

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