Haplotype-Based Association of Four Lymphotoxin-Alpha Gene Polymorphisms with the Risk of Coronary Artery Disease in Han Chinese

Liu, Yan; Sheng, Haihui; Lü, Lin; Wu, Zhijun; Chen, Qiujin; Xiao, Huasheng; Jin, Wei

doi:10.1620/tjem.224.119

Cited by 8 publications

(9 citation statements)

References 41 publications

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“…In these regression models the predictors explained from 12.9% to 17.2% of the variance in pain intensity outcomes. The test for interaction between TNF/LTA region SNPs and depressive symptoms revealed that depression was positively associated with pain intensity only in one of the genotype groups (CC at rs2229094) and in the expected direction of association, as the C allele has been associated with increased risk of inflammation-related traits (22,36). The C allele encodes a predicted amino acid substitution in a transmembrane domain and thus could feasibly alter protein function (33).…”

Section: Discussionmentioning

confidence: 98%

Inflammatory Genes and Psychological Factors Predict Induced Shoulder Pain Phenotype

George

Parr

Wallace

et al. 2014

Medicine &Amp; Science in Sports &Amp; Exercise

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Purpose The pain experience has multiple influences but little is known about how specific biological and psychological factors interact to influence pain responses. The current study investigated the combined influences of genetic (pro-inflammatory) and psychological factors on several pre-clinical shoulder pain phenotypes. Methods An exercise-induced shoulder injury model was used, and a priori selected genetic (IL1B, TNF/LTA region, IL6 single nucleotide polymorphisms, SNPs) and psychological (anxiety, depressive symptoms, pain catastrophizing, fear of pain, kinesiophobia) factors were included as the predictors of interest. The phenotypes were pain intensity (5-day average and peak reported on numerical rating scale), upper-extremity disability (5-day average and peak reported on the QuickDASH instrument), and duration of shoulder pain (in days). Results After controlling for age, sex, and race, the genetic and psychological predictors were entered separately as main effects and interaction terms in regression models for each pain phenotype. Results from the recruited cohort (n = 190) indicated strong statistical evidence for the interactions between 1) TNF/LTA SNP rs2229094 and depressive symptoms for average pain intensity and duration and 2) IL1B two-SNP diplotype and kinesiophobia for average shoulder pain intensity. Moderate statistical evidence for prediction of additional shoulder pain phenotypes included interactions of kinesiophobia, fear of pain, or depressive symptoms with TNF/LTA rs2229094 and IL1B. Conclusion These findings support the combined predictive ability of specific genetic and psychological factors for shoulder pain phenotypes by revealing novel combinations that may merit further investigation in clinical cohorts, to determine their involvement in the transition from acute to chronic pain conditions.

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Section: Discussionmentioning

confidence: 98%

Inflammatory Genes and Psychological Factors Predict Induced Shoulder Pain Phenotype

George

Parr

Wallace

et al. 2014

Medicine &Amp; Science in Sports &Amp; Exercise

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“…The LTA variants are shown to be associated with cancer risks under different genetic models. These genetic models consist of additive (per variant allele vs. common allele), dominant (variant allele carriers vs. homozygotes for the common allele) and recessive (homozygotes for the variant allele vs. all others) genetic models [64,65]. LTA rs1041981 is associated with a significantly lower presence of Japanese male lung cancer under the dominant model (CA+AA versus CC) [28]; LTA rs909253 is associated with high risk of Asian gastric cancer in the heterozygote comparison (GA versus AA) [15]; LTA rs2009658 is shown to be associated with significantly elevated risk of breast cancer among Caucasian women aged 45–64 years under the additive model (C versus G) [51].…”

Section: Discussionmentioning

confidence: 99%

Four Genetic Polymorphisms of Lymphotoxin-Alpha Gene and Cancer Risk: A Systematic Review and Meta-Analysis

Huang

Wang

et al. 2013

PLoS ONE

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Lymphotoxin-alpha (LTA) is a pro-inflammatory cytokine that plays an important role in the inflammatory and immunologic response. Numerous studies have shown LTA polymorphisms as risk factors for cancers, but the results remain inconclusive. The goal of the present meta-analyses is to establish the associations between cancers and four LTA variants (rs1041981, rs2239704, rs2229094 and rs746868). A total of 30 case-control studies involving 58,649 participants were included in the current meta-analyses. Our results showed significant associations with increased cancer risk for rs1041981 (odd ratio (OR) = 1.15, 99% confidential interval (CI) = 1.07-1.25, P < 0.0001, I2 = 12.2%), rs2239704 (OR = 1.08, 99% CI = 1.01-1.16, P = 0.021, I2 = 0.0%) and rs2229094 (OR = 1.28, 99% CI = 1.09-1.50, P = 0.003, I2 = 0.0%). No evidence was found for the association between rs746868 and cancer risk (OR = 1.01, 99% CI = 0.93-1.10, P = 0.771, I2 = 0.0%). Subgroup meta-analysis suggested that rs2239704 was likely to increase the risk of hematological malignancy (OR = 1.10, 99% CI = 1.01–1.20, P = 0.023, I2 = 0.0%), and rs2229094 was specific for the increased risk of adenocarcinoma (OR = 1.33, 99% CI = 1.11-1.59, P = 0.002, I2 = 0.0%). In conclusion, our meta-analyses suggested that the LTA rs1041981, rs2239704 and rs2229094 polymorphisms contributed to the increased risk of cancers. Future functional studies were needed to clarify the mechanistic roles of the three variants in the cancer risk.

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“…LT is essential for controlling intracellular bacterial infections (56) and contributes to atherosclerosis in mice (61). Genetic variations in LT or the TNF-LTA locus in specific human populations are associated with decreased insulin resistance (21), dyslipidemia in rheumatoid arthritis patients (58), type 2 diabetes (38), and risk of coronary artery disease (30).…”

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confidence: 99%

Deficiency of lymphotoxin-α does not exacerbate high-fat diet-induced obesity but does enhance inflammation in mice

Pamir

McMillen

Edgel

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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(LT␣) is secreted by lymphocytes and acts through tumor necrosis factor-␣ receptors and the LT␤ receptor. Our goals were to determine whether LT has a role in obesity and investigate whether LT contributes to the link between obesity and adipose tissue lymphocyte accumulation. LT deficient (LT Ϫ/Ϫ ) and wild-type (WT) mice were fed standard pelleted rodent chow or a high-fat/high-sucrose diet (HFHS) for 13 wk. Body weight, body composition, and food intake were measured. Glucose tolerance was assessed. Systemic and adipose tissue inflammatory statuses were evaluated by quantifying plasma adipokine levels and tissue macrophage and T cell-specific gene expression in abdominal fat. LT Ϫ/Ϫ mice were smaller (20%) and leaner (25%) than WT controls after 13 wk of HFHS diet feeding. LT Ϫ/Ϫ mice showed improved glucose tolerance, suggesting that, in WT mice, LT may impair glucose metabolism. Surprisingly, adipose tissue from rodent chow-and HFHS-fed LT Ϫ/Ϫ mice exhibited increased T lymphocyte and macrophage infiltration compared with WT mice. Despite the fact that LT Ϫ/Ϫ mice exhibited an enhanced inflammatory status at the systemic and tissue level even when fed rodent chow, they were protected from enhanced diet-induced obesity and insulin resistance. Thus, LT contributes to body weight and adiposity and is required to modulate the accumulation of immune cells in adipose tissue.

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Haplotype-Based Association of Four Lymphotoxin-Alpha Gene Polymorphisms with the Risk of Coronary Artery Disease in Han Chinese

Cited by 8 publications

References 41 publications

Inflammatory Genes and Psychological Factors Predict Induced Shoulder Pain Phenotype

Inflammatory Genes and Psychological Factors Predict Induced Shoulder Pain Phenotype

Four Genetic Polymorphisms of Lymphotoxin-Alpha Gene and Cancer Risk: A Systematic Review and Meta-Analysis

Deficiency of lymphotoxin-α does not exacerbate high-fat diet-induced obesity but does enhance inflammation in mice

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