scholarly journals SOCS3 Gene Polymorphism and Hypertension Susceptibility in Chinese Population: A Two-Center Case-Control Study

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Dabin Kuang ◽  
Lichen Dong ◽  
Lingyun Liu ◽  
Meiling Zuo ◽  
Yuanlin Xie ◽  
...  
Keyword(s):  
Chinese Population ◽  
Mrna Level ◽  
Taqman Assay ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Healthy Donors ◽  
Increased Risk ◽  
Socs3 Mrna ◽  
Control Study ◽  
Inflammatory Effect

Endothelial inflammation and vascular damage are essential risk factors contributing to hypertension. Suppressor of cytokine signaling 3 (SOCS3) is involved in the regulation of multiple inflammatory pathways. A large number of studies have shown that the anti-inflammatory effect of SOCS3 in hypertension, obesity, and allergic reactions has brought more insights into the inhibition of inflammation. Therefore, we selected a tagSNP of SOCS3 (rs8064821) to investigate whether they are contributing to the risk of hypertension in the Chinese population. In total, 532 patients with hypertension and 569 healthy controls were enrolled for two central of China. SOCS3 rs8064821 C>A polymorphism was genotyped using TaqMan assay. SOCS3 rs8064821 CA genotype was associated with an increased risk of hypertension ( OR = 1.821 , 95 % CI = 1.276 -2.600, P = 0.001 ). Rs8064821 A allele was associated with higher SOCS3 mRNA level in PBMCs from healthy donors. SOCS3 rs8064821 C>A polymorphism may contribute to the risk of hypertension in the Chinese population by regulating the expression of SOCS3.

scholarly journals Genetic Variants in KIR/HLA-C Genes Are Associated With the Susceptibility to HCV Infection in a High-Risk Chinese Population

2021 ◽  
Vol 12 ◽  
Author(s):  
Chao Shen ◽  
Zhijun Ge ◽  
Chen Dong ◽  
Chunhui Wang ◽  
Jianguo Shao ◽  
...  
Keyword(s):  
High Risk ◽  
Chinese Population ◽  
Drug Users ◽  
Hcv Infection ◽  
Taqman Assay ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Risk Alleles ◽  
Increased Risk ◽  
Control Study

BackgroundKIR/HLA-C signaling pathway influences the innate immune response which is the first defense to hepatitis C virus (HCV) infection. The aim of this study was to determine the association between the genetic polymorphisms of KIR/HLA-C genes and the outcomes of HCV infection in a high-risk Chinese population.MethodsIn this case-control study, four single nucleotide polymorphisms (SNPs) of KIR/HLA-C genes (KIR2DS4/KIR2DS1/KIR2DL1 rs35440472, HLA-C rs2308557, HLA-C rs1130838, and HLA-C rs2524094) were genotyped by TaqMan assay among drug users and hemodialysis (HD) patients including 1,378 uninfected control cases, 307 subjects with spontaneous viral clearance, and 217 patients with persistent HCV infection. Bioinformatics analysis was used to functionally annotate the SNPs.ResultsAfter logistic regression analysis, the rs35440472-A and rs1130838-A alleles were found to be associated with a significantly elevated risk of HCV infection (OR = 1.562, 95% CI: 1.229–1.987, P < 0.001; OR = 2.134, 95% CI: 1.180–3.858, P = 0.012, respectively), which remained significant after Bonferroni correction (0.05/4). The combined effect of their risk alleles and risk genotypes (rs35440472-AA and rs1130838-AA) were linked to the increased risk of HCV infection in a locus-dosage manner (all Ptrend < 0.001). Based on the SNPinfo web server, rs35440472 was predicted to be a transcription factor binding site (TFBS) while rs1130838 was predicted to have a splicing (ESE or ESS) function.ConclusionKIR2DS4/KIR2DS1/KIR2DL1 rs35440472-A and HLA-C rs1130838-A variants are associated with increased susceptibility to HCV infection in a high-risk Chinese population.

scholarly journals PTPN22 Gene Polymorphisms Are Associated with Susceptibility to Large Artery Atherosclerotic Stroke and Microembolic Signals

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Lingyan Zhou ◽  
Kun Wang ◽  
Junhong Wang ◽  
Zhenfeng Zhou ◽  
Yufei Cheng ◽  
...  
Keyword(s):  
Protein Tyrosine Phosphatase ◽  
Odds Ratio ◽  
Chinese Population ◽  
Interaction Analysis ◽  
Tyrosine Phosphatase ◽  
Taqman Assay ◽  
Large Artery ◽  
Ptpn22 Gene ◽  
Increased Risk ◽  
The Relationship

Large artery atherosclerotic stroke (LAAS) is the most common ischemic stroke (IS) subtype, and microemboli may be clinically important for indicating increased risk of IS. The inflammatory process of atherosclerosis is well known, and lymphoid phosphatase (Lyp), which is encoded by the protein tyrosine phosphatase nonreceptor type 22 (PTPN22) gene, plays an important role in the inflammatory response. Our study was intended to evaluate the relationship between PTPN22 gene and LAAS and microembolic signals (MES). Three loci of the PTPN22 gene (rs2476599, rs1217414, and rs2488457) were analyzed in 364 LAAS patients and 369 control subjects. A genotyping determination was performed using the TaqMan assay. The G allele of rs2488457 might be related to a higher risk for developing LAAS and MES (odds ratio OR=1.456, 95% confidence interval (CI) 1.156-1.833, P=0.001; OR=1.652, 95% CI 1.177-2.319, P=0.004, respectively). In the LAAS group, the prevalence of the GTG haplotype was higher (P<0.001) and the prevalence of the GCC haplotype was lower (P=0.001). An interaction analysis of rs2488457 with smoking showed that smokers with the CG/GG genotypes had a higher risk of LAAS, compared to nonsmokers with the rs2488457 CC genotype (OR=2.492, 95% CI 1.510–4.114, P<0.001). Our research indicated that the PTPN22 rs2488457 might be related to the occurrence of LAAS and MES in the Han Chinese population. In addition, the rs2488457 polymorphism and the environmental factor of smoking jointly influenced the susceptibility of LAAS.

scholarly journals CD40 polymorphisms were associated with HCV infection susceptibility among Chinese population

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ting Tian ◽  
Peng Huang ◽  
Jingjing Wu ◽  
Chunhui Wang ◽  
Haozhi Fan ◽  
...  
Keyword(s):  
Chinese Population ◽  
Pairwise Comparison ◽  
Cross Sectional Study ◽  
Recessive Model ◽  
Hcv Infection ◽  
Taqman Assay ◽  
Cross Sectional ◽  
Antiviral Immune Response ◽  
Logistic Analysis ◽  
Increased Risk

Abstract Background CD40, encoded by TNFRSF5, participates in the survival of B cells, process of antigen presentation and generation of CD8+ T cell memory. It also has an important effect on HCV antiviral immune response. This study aims to investigate whether TNFRSF5 gene polymorphisms are associated with HCV infection outcomes among Chinese population. Methods Three single nucleotide polymorphism (SNPs) (rs1535045, rs1883832, rs4810485) on TNFRSF5 were genotyped by TaqMan assay among Chinese population, including 1513 uninfected subjects, 496 spontaneous viral clearance subjects and 768 persistent HCV-infected subjects. Logistic analysis was used to compare these SNPs among different groups in this cross-sectional study. Functional annotations of the identified SNPs were further evaluated by bioinformatics analysis. Results After adjusted by age, gender and routes of infection, the results of logistic analysis indicated that individuals carrying rs1535045 T allele had a higher risk to infect HCV compared with C allele (in recessive model, adjusted OR = 1.368, 95%CI = 1.070-1.749, P = 0.012). Subjects carried rs1535045 TT genotype were more likely to infect HCV than wild CC genotype (adjusted OR = 1.397, 95%CI = 1.078-1.809, P = 0.011). For rs1883832, T allele was significantly associated with an increased risk of HCV infection (in recessive model, adjusted OR = 1.337, 95%CI = 1.069-1.673, P = 0.011). Subjects with TT genotype had more possibility to infect HCV (adjusted OR = 1.351, 95%CI = 1.060-1.702, P = 0.015). In the stratified analysis, rs1535045 and rs1883832 were remained in various subgroups and the heterogeneity test showed no pronounced heterogeneity in any pairwise comparison (all P > 0.05). In addition, the results of the cumulative effects showed a tendency of that the more risk alleles (rs1535045 T and rs1883832 T) subjects carried, the more possibility of HCV infection exhibited (P<0.001). In haplotype analyses, compared with the CC haplotype, CT, TC and TT was correlated with an increased risk to infect HCV (P = 0.029, P = 0.047 and P<0.001, respectively). Conclusions In conclusion, CD40 polymorphisms were significantly associated with the susceptibility to HCV among Chinese populations.

scholarly journals Association of lncRNA PVT1 Gene Polymorphisms with the Risk of Essential Hypertension in Chinese Population

2022 ◽  
Vol 2022 ◽  
pp. 1-9
Author(s):  
Rong Li ◽  
Xia Yu ◽  
Yang Chen ◽  
Mulun Xiao ◽  
Meiling Zuo ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Chinese Population ◽  
Vascular Dysfunction ◽  
Blood Lipid ◽  
Chinese Patients ◽  
Taqman Assay ◽  
Tumor Tissues ◽  
Increased Risk ◽  
Variant Translocation ◽  
Blood Lipid Levels

Vascular dysfunction and hyperlipidemia are essential risk factors contributing to essential hypertension (EH). The plasmacytoma variant translocation 1 (PVT1) is involved in modulating angiogenesis in tumor tissues and plays an important role in fat differentiation in the progress of obesity. Therefore, we selected two tagSNPs of PVT1 (rs10956390 and rs80177647) to investigate whether they are contributing to the risk of hypertension in Chinese patients. In total, 524 adult patients with EH and 439 matched healthy controls were enrolled for two central of China. Results. PVT1 rs10956390 and rs80177647 polymorphisms were genotyped by using TaqMan assay. PVT1 rs10956390 TT genotype was associated with a decreased risk of EH ( OR = 0.561 , 95% CI = 0.372 -0.846, P = 0.006 ), while rs80177647 TA genotype was associated with an increased risk ( OR = 2.236 , 95% CI = 1.515 -3.301, P < 0.001 ). Rs10956390 T allele was associated with lower triglyceride levels in the plasma both from healthy and EH donors. What is more, there is an association between rs10956390 polymorphism and HDL-C level, as well as LDL-C. Conclusion. PVT1 rs10956390 and rs80177647 polymorphisms may contribute to the risk of EH in Chinese population by regulating blood lipid levels.

MiR-221 Regulates Suppressors of Cytokine Signaling 3-Janus Kinase 2/Signal Transducer and Activator of Transcription 3 (SOCS3-JAK2/STAT3) Pathway and Affects Thyroid Cancer Cell Proliferation and Apoptosis

2022 ◽  
Vol 12 (5) ◽  
pp. 996-1001
Author(s):  
Neng Jiang ◽  
Shunfu Zhu ◽  
Jianjun Zhu
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Mrna Level ◽  
Cytokine Signaling ◽  
Thyroid Cancer Cell ◽  
Tumor Tissues ◽  
Proliferation And Apoptosis ◽  
Socs3 Expression ◽  
Thyroid Cancer Cells ◽  
Socs3 Mrna

Objective: Suppressors of cytokine signaling 3 (SOCS3) negatively regulates JAK-STAT signaling. Bioinformatics analysis showed a targeted relationship between miR-221 and SOCS3 mRNA 3′-UTR. This study investigated whether miR-221 regulates SOCS3 expression and affects thyroid cancer cells. Methods: Dual-luciferase reporter gene experiments verified the relationship between miR-221 and SOCS3. The tumor tissues and adjacent tissues of patients with thyroid cancer were collected to detect miR-221 and SOCS3 level. Thyroid cancer cell line KTC-1 cells were assigned into miR-NC group and miR-221 inhibitor group followed by analysis of SOCS3, p-JAK2, and p-STAT3 level by Real-time PCR, cell apoptosis and cell proliferation by flow cytometry and cell invasion by Transwell assay. Results: Compared with adjacent tissues, miR-221 level in tumor tissues was increased, and SCOS3 mRNA level was decreased. There was a targeted relationship between miR-221 and SOCS3 mRNA. MiR-221 level in KTC-1 and TPC-1 cells was increased, while SOCS3 mRNA level was decreased. MiR-221 inhibitor can significantly upregulate SOCS3 mRNA and protein in KTC-1 cells, reduce the expression of p-JAK2, p-STAT3 protein, increase cell apoptosis, and reduce cell proliferation and invasion. Conclusion: The increased miR-221 and decreased SOCS3 expression are related to thyroid cancer pathogenesis. MiR-221 can inhibit the expression of SOCS3, affect JAK-STAT signaling activity, and regulate the proliferation and apoptosis of thyroid cancer cells.

scholarly journals Leishmania donovani-Induced Expression of Suppressor of Cytokine Signaling 3 in Human Macrophages: a Novel Mechanism for Intracellular Parasite Suppression of Activation

2003 ◽  
Vol 71 (4) ◽  
pp. 2095-2101 ◽  
Author(s):  
Sylvie Bertholet ◽  
Harold L. Dickensheets ◽  
Faruk Sheikh ◽  
Albert A. Gam ◽  
Raymond P. Donnelly ◽  
...  
Keyword(s):  
Leishmania Donovani ◽  
De Novo ◽  
Polymyxin B ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Factor Alpha ◽  
Kinetics Of ◽  
Socs3 Mrna

ABSTRACT Leishmania donovani protozoan parasites, the causative agent of visceral leishmaniasis, establish an infection partly by interfering with cytokine signaling in the host macrophages. Therefore, we investigated the expression of the suppressor of cytokine signaling (SOCS) genes in human macrophages infected with L. donovani. The expression of SOCS3 mRNA was induced transiently after exposure to live or heat-killed parasites, but not purified lipophosphoglycan, while that of other SOCS genes remained unchanged. SOCS3 gene expression was not dependent on phagocytosis or on cytokines released by L. donovani-infected macrophages, such as interleukin-1β or tumor necrosis factor alpha. In addition, Leishmania used a different signaling pathway(s) than bacterial lipopolysaccharide to induce SOCS3 mRNA, as indicated by the kinetics of induction and sensitivity to polymyxin B inhibition. Finally, phosphorylation of the STAT1 transcription factor was significantly reduced in L. donovani-infected macrophages and required de novo transcription. The induction of SOCS3 provides a potent inhibitory mechanism by which intracellular microorganisms may suppress macrophage activation and interfere with the host immune response.

scholarly journals Single-Nucleotide Polymorphisms in XPO5 are Associated with Noise-Induced Hearing Loss in a Chinese Population

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Ning Wang ◽  
Boshen Wang ◽  
Jiadi Guo ◽  
Suhao Zhang ◽  
Lei Han ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Chinese Population ◽  
Luciferase Reporter ◽  
Noise Induced Hearing Loss ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Increased Risk ◽  
Polymerase Chain ◽  
Control Study ◽  
Dual Luciferase Reporter Assay

Objectives.The purpose of this study was to investigate the correlation between single-nucleotide polymorphism (SNP) in 3′UTR of XPO5 gene and the occurrence of noise-induced hearing loss (NIHL), and to further explore the regulatory mechanism of miRNAs in NIHL on XPO5 gene. Methods.We conducted a case-control study involving 1040 cases and 1060 controls. The effects of SNPs on XPO5 expression were studied by genotyping, real-time polymerase chain reaction (qPCR), cell transfection, and the dual-luciferase reporter assay. Results.We genotyped four SNPs (rs2257082, rs11077, rs7755135, and rs1106841) in the XPO5 gene. The rs2257082 AG/GG carriers have special connection to an increased risk of noise-induced hearing loss compared to the AA carriers. The rs11077TG/GG carriers had a significantly increased association with NIHL susceptibility than the TT carriers. There was a higher risk of NIHL in the XPO5 gene rs7755135 CC carriers than in the TT carriers. No statistically significant correlation was obtained with respect to SNPrs1106841. Functional experiments showed that the rs11077 change might inhibit the interaction between miRNAs (miRNA-4763-5p, miRNA-5002-3p, and miRNA-617) and XPO5, with rs11077G allele resulting in overexpression of XPO5. Conclusion. The genetic polymorphism, rs11077, within XPO5 is associated with the risk of noise-induced hearing loss in a Chinese population.

Association between polymorphisms inIL27and risk for CHD in a Chinese population

2015 ◽  
Vol 26 (2) ◽  
pp. 237-243 ◽  
Author(s):  
Danyan Zhang ◽  
Mingfu Ma ◽  
Yuyou Yang ◽  
Ling Wan ◽  
Zhixi Yang ◽  
...  
Keyword(s):  
Ventricular Septal Defect ◽  
Atrial Septal Defect ◽  
Chinese Population ◽  
Septal Defect ◽  
Fragment Length Polymorphism ◽  
Chd Risk ◽  
Increased Risk ◽  
Polymerase Chain ◽  
Maternal Tolerance ◽  
Control Study

AbstractBackgroundIL-27, a member of the IL-12 family, has been involved in maternal tolerance to the foetus and successful pregnancy. Growing evidences indicate that IL-27 plays a crucial role in pregnancy.AimWe carried out the present study in order to investigate whether polymorphisms in theIL27are associated with the risk for CHDs, including atrial septal defect and ventricular septal defect.Patients and methodsWe conducted this case–control study among 247 atrial septal defect patients, 150 ventricular septal defect patients, and 368 healthy controls in a Chinese population using polymerase chain reaction-restriction fragment length polymorphism assay.ResultsSignificantly increased risk for atrial septal defect (p=0.001, OR=1.490, 95% CI=1.178–1.887) and ventricular septal defect (p=0.004, OR=1.502, 95% CI=1.139–1.976) was observed to be associated with the allele G of rs153109. In a dominant model, we have also observed that increased susceptibilities for atrial septal defect (p<0.01, OR=1.89, 95% CI=1.35–2.63) and ventricular septal defect (p<0.01, OR=2.50, 95% CI=1.67–3.85) were statistically associated with rs153109; however, no association was found between CHD risk and rs17855750 in theIL27gene.ConclusionThe 153109 of theIL27gene may be associated with the susceptibility to CHD, including atrial septal defect and ventricular septal defect.

Prestroke Statins Improve Prognosis of Atrial Fibrillation-Associated Stroke through Increasing Suppressor of Cytokine Signaling-3 Levels

2021 ◽  
pp. 1-7
Author(s):  
Taoli Lu ◽  
Xu Yang ◽  
Yanli Cai ◽  
Chenchen Xie ◽  
Bei Zhang
Keyword(s):  
Atrial Fibrillation ◽  
Clinical Outcomes ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Mortality And Morbidity ◽  
Statin Group ◽  
Medical Centers ◽  
Increased Risk ◽  
Electrocardiogram Monitoring ◽  
Metalloproteinase 9

Background: Cerebral infarction associated with atrial fibrillation (AF) has relatively higher mortality and morbidity rates than other types of stroke. Statins are being commonly prescribed to patients with stoke. However, the use of statins in AF-related stroke, especially prestroke, has not been well studied. This study aimed to investigate whether the use of prestroke statins could improve clinical outcomes in patients with AF-related acute ischemic stroke (AIS) and its mechanism. Methods: This prospective study enrolled 453 AF-associated AIS patients from 4 medical centers and divided them into 2 groups based on the statin use before the stroke episode. All patients received comprehensive clinical examinations including 72-h Holter electrocardiogram monitoring and were followed up for 3 months. Plasma suppressor of cytokine signaling-3 (SOCS-3) and matrix metalloproteinase-9 (MMP-9) levels were measured by ELISA on admission and days 3 and 7 after enrollment. The endpoints were death, major disability (modified Rankin Scale score ≥3), and composite outcome (death/major disability) at 3 months after the AIS episode. Results: Plasma SOCS-3 levels were significantly increased and MMP-9 levels decreased in patients in the prestroke statin group on hospital admission and days 3 and 7 after enrollment (p < 0.001). Furthermore, our data suggested that baseline plasma SOCS-3 levels were associated with increased risk of 3-month mortality (adjusted odds ratio [OR], 1.012; 95% confidence interval [CI], 1.006–1.018; p < 0.001) and major disability (adjusted OR, 1.013; 95% CI, 1.007–1.02; p < 0.001). Similarly, baseline plasma MMP-9 levels were also associated with increased risk of 3-month mortality (adjusted OR, 1.037; 95% CI, 1.022–1.053; p < 0.001) and major disability (adjusted OR, 1.038; 95% CI, 1.022–1.55; p < 0.001). Conclusion: Our data suggested that the prestroke use of statins improved the clinical outcomes in AIS patients with AF by upregulating the level of SOCS-3 and reducing the plasma MMP-9 level.

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