Monocyte chemoattractant protein-1 (MCP-1)-2518?A/G polymorphism and lupus nephritis risk: A PRISMA-compliant meta-analysis.
Ontology highlight
ABSTRACT:
SUBMITTER: Sang GY
PROVIDER: S-EPMC5758254 | biostudies-other | 2017 Dec
REPOSITORIES: biostudies-other
Publications
Monocyte chemoattractant protein-1 (MCP-1)-2518 A/G polymorphism and lupus nephritis risk: A PRISMA-compliant meta-analysis.
Sang Guo-Yao GY Meng Cun-Ren CR Hao Yun-Fei YF Dai Jiang-Hong JH
Medicine 20171201 51
<h4>Background</h4>Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the development of allergic inflammatory reactions by recruiting various immune cells, which is associated with many autoimmune diseases, but the association with the MCP-1-2518A/G gene polymorphism and lupus nephritis (LN) was still controversial in previous studies. Thus, we performed a meta-analysis to derive a more precise evaluation of the association between MCP-1 -2518A/G polymorphism and LN risk and ...[more]
Similar Datasets
Project description:BackgroudMycophenolate mofetil (MMF) has been recommended for the treatment of lupus nephritis (LN). Although inter-racial differences exist regarding the appropriate dose and efficacy of MMF in patients with LN, no definitive meta-analysis has yet been conducted in Chinese patients. This analysis investigated the efficacy and safety of MMF in Chinese patients with proliferative LN.MethodsA systematic literature search was conducted to select randomized controlled trials that reported at least one of the following: complete remission (CR), partial remission, total remission (TR; defined as complete remission + partial remission), relapse rate, serum creatinine, creatinine clearance, end-stage renal disease, death, infections, amenorrhea, leukopenia, alopecia, gastrointestinal symptoms, or liver damage.ResultsEighteen trials (927 patients) were included; 14 (750 patients) reported CR, partial remission, and TR. Two trials (58 patients) reported relapse rates during maintenance treatment. MMF induction significantly improved CR and TR vs cyclophosphamide (relative risk 1.34, 95% confidence interval: 1.13-1.58; P < .001; relative risk 1.16, 95% confidence interval: 1.02-1.33; P = .03), and was associated with significantly lower risks of infection (P < .001), amenorrhea (P < .001), leukopenia, and alopecia. No significant difference in relapse rate was evident between the MMF and azathioprine groups (P = .66).ConclusionAccording to this meta-analysis of 18 trials, MMF is significantly more effective than cyclophosphamide induction, and is associated with reduced incidences of infections, amenorrhea, leukopenia, and alopecia in Chinese patients with proliferative LN.
| S-EPMC7437744 | biostudies-literature
Project description:BACKGROUND:ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development. However, whether ISL1 rs1017 polymorphism is associated with the congenital heart disease (CHD) risk remains controversial. METHODS:Five database including PubMed, Cochrane Library, ISI Web of Science, CNKI, and Wan Fang were searched by using key words "Insulin Gene Enhancer Protein ISL1" and "Single Nucleotide Polymorphism," and "Congenital Heart Disease." Five relative articles including 6 independent studies containing 2132 cases and 3812 controls were finally recruited to our study. Meta-analyses were performed by pooling odds ratios (ORs) and 95% confidence interval (CI) from included studies using STATA 12.0 software. RESULTS:The associations between ISL1 rs1017 polymorphism and the risk of CHD were statistically significant under the allele model (T vs A; OR: 1.421; 95% CI: 1.072-1.882), heterozygous model (AT vs AA; OR: 1.342; 95% CI: 1.019-1.767), and dominant model (AT+ TT vs AA; OR: 1.466; 95% CI: 1.059-2.028). Sensitivity analysis indicated that the results were not stable. Subgroup analysis demonstrated that associations were found in Caucasians under the allele model and the heterozygous model (P?<?.05), but not the dominant model (P?>?.05). CONCLUSION:In summary, our meta-analysis results suggest that the T allele of ISL1 rs1017 is a risk factor for CHD. However, further studies based on large sample size and multi-ethnic population should be conducted to further prove this correlation.
| S-EPMC6959884 | biostudies-literature
Project description:BACKGROUND:Cyclooxygenase-2 (COX-2) is an inducible enzyme that mediates the synthesis of prostaglandin, which plays an important role in the inflammation response. The overexpression of COX-2 in lung cancer has been found in several studies, suggesting that COX-2 contributes to carcinogenesis. There are many previous case-control studies focused on the association between COX-2 polymorphism and lung cancer risk, however, the conclusion remained controversial. OBJECTIVES:We performed this meta-analysis to evaluate the association between COX-2 rs5275 and rs689466 polymorphism and susceptibility to lung cancer. METHODS:A systematic literature research was conducted on PubMed, Embase, Cochrane Library, OVID, Web of Science, and Google Scholar up to November 30, 2017. The quality of studies was assessed by Newcastle-Ottawa scale. We combined odds ratios (ORs) and 95% confidence intervals (CIs) in 5 different genetic models for evaluation under a fixed-effect model or random-effect model. Subgroup analysis was performed according to source of control, ethnicity, pathological types, and smoking status. Sensitivity analysis and publication bias were also conducted. RESULTS:Eventually, 14 eligible studies were included in our meta-analysis. We found rs5275 gene polymorphism decreased the risk of lung cancer under heterozygote model (OR: 0.91, 95% CI: 0.84-0.98, P?=?.02). COX-2 rs689466 gene polymorphism was also related to a significantly reduced risk under allele (OR: 0.88, 95% CI: 0.82-0.95, P?=?.001), homozygote (OR: 0.81, 95% CI: 0.68-0.95, P?=?.01), heterozygote (OR: 0.81, 95% CI: 0.72-0.91, P?<?.001), and dominant model (OR: 0.81, 95% CI: 0.72-0.91, P?<?.001), except for recessive model. Subgroup analysis suggested a similar association in Asians, but not in Caucasians. Polymorphism of rs5275 was strongly associated with a reduced risk of lung adenocarcinoma according to stratified analysis by pathological types. Egger test identified no significant publication bias. CONCLUSIONS:Our meta-analysis demonstrated that COX-2 rs5275 and rs689466 polymorphism significantly decrease the risk of lung cancer in Asians but not in Caucasians, indicating COX-2 could serve as a potential diagnostic marker for lung cancer.
| S-EPMC6393127 | biostudies-literature
Project description:BackgroundPrevious case-control studies on association between KCNE1 G38S polymorphism and risk of atrial fibrillation (AF) have been published but because of the conflicting results and small sample size of individual studies, the consolidated result is still controversial.ObjectivesThe aim of this study was to explore the relationship between KCNE1 G38S polymorphism and risk of AF.MethodsWe performed a comprehensive literature search on PubMed, Embase, OVID, Web of Science, Wan Fang, and CNKI databases up to March 10, 2017 in English and Chinese languages. Two of the authors individually extracted study data and assessed the study quality using Newcastle-Ottawa scale. Odds ratios (ORs) and 95% confidence intervals (CIs) were combined in different genetic models for evaluation using a random-effect model or fixed-effect model according to interstudy heterogeneity.ResultsThere were totally 14 independent case-control studies of 2810 patients and 3080 healthy controls included. Significant associations were found between KCNE1 G38S polymorphism and AF in overall population under all genetic models: allelic (OR: 1.34, 95% CI: 1.24-1.45, P < .001), homozygous (OR: 1.90, 95% CI: 1.61-2.24, P < .001), heterozygous (OR: 1.43, 95% CI: 1.21-1.68, P < .001), recessive (OR: 1.42, 95% CI: 1.20-1.69, P < .001), dominant genetic model (OR: 1.62, 95% CI: 1.39-1.89, P < .001). Subgroup analyses indicated similar association in Chinese and white.ConclusionsThe G38S polymorphism in the KCNE1 gene can significantly increase the risk of AF in both Chinese and white.
| S-EPMC5484235 | biostudies-literature
Project description:Background and objectivemiRNA-146a is a microRNA that plays an important role in systemic lupus erythematosus (SLE). Several studies have examined the role of miRNA-146a in SLE, but have demonstrated equivocal or even contradictory conclusions. Therefore, this meta-analysis aimed to assess the role of miRNA-146a in SLE by examining data from previous studies.MethodsA meta-analysis of relevant papers published before August 31, 2019, in the WanFang, Chinese Biomedical Literature Database (CBM), Chinese National Knowledge Infrastructure (CNKI), PubMed, EMBASE, and Web of Science databases was performed to verify the relationship of miRNA-146a expression level to SLE. Two investigators independently extracted the data and conducted a quality assessment of the studies. All statistical analyses were performed using Stata 14.0. Trial sequence analysis (TSA) was conducted to assess the quality and strength of the studies using the TSA software.ResultsSix publications, involving 151 SEL patients and 132 healthy individuals as controls were included in this meta-analysis. The results showed that the expression of miRNA-146a was associated with SLE risk [standard mean difference (SMD) = -1.21, 95% confidence interval (95% CI) (-2.18, -0.23), P = .015]. The stratified analysis revealed that the expression of miRNA-146a was highly related to higher SLE risk among Asian (SMD = -1.30, 95% CI (-2.52, -0.07), P = .038) and Caucasian (SMD = -0.72, 95% CI (-1.20, -0.24), P = .003) populations. Besides, the serum levels of miRNA146a were significantly different (SMD = -1.73, 95% CI (-3.11, -0.36), P = .014). The TSA revealed that the cumulative Z-curve crossed the typical boundary value, and reached the TSA monitoring boundary, but did not reach the required information size. This indicates that even if the cumulative sample size did not meet required information size, no more trials were needed and a reliable conclusion was reached in advance. Sensitivity analyses indicated the instability of the meta-analysis.ConclusionsOverall, the expression of miRNA-146a is associated with SLE risk. Therefore, miRNA-146a is a promising candidate for the effective diagnosis of SLE. But, due to the limitations of this study, it is necessary to cautiously explain the results of this study.Systematic review registrationPROSPERO CRD42019151381.
| S-EPMC7535641 | biostudies-literature
Project description:BackgroundA dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis is closely related to the occurrence of depression. The glucocorticoid receptor, also known as the nuclear receptor subfamily 3, group C, member 1 (NR3C1), provides negative feedback to the HPA axis by binding to glucocorticoids. Some studies have demonstrated an association between the NR3C1 rs41423247 polymorphism and depression, but results from other studies have been controversial.MethodIn this study, the association between the NR3C1 rs41423247 polymorphism and depression was evaluated by a meta-analysis using the RevMan 5.3 software, and the Stata 10.0 software was used for sensitivity analysis and publication bias test. According to the inclusion criteria, related studies in databases were retrieved and screened.ResultsIn total, 9 articles were selected, including 1630 depressed patients and 3362 controls. The meta-analysis showed that homozygous mutation of NR3C1 rs41423247 was associated with depression in the total population (OR = 0.77, 95% CI = 0.64-0.94, P = .01) and in Caucasians (OR = 0.78, 95% CI = 0.63-0.96, P = .02).ConclusionThis meta-analysis demonstrates that the NR3C1 rs41423247 homozygous mutation may be a risk factor for depression.
| S-EPMC6181539 | biostudies-literature
Project description:OBJECTIVE:Numerous studies have evaluated the association between the rs2187668 polymorphism in the human leucocyte antigen (HLA) complex class II HLA-DQ a-chain 1 (HLA-DQA1) gene and idiopathic membranous nephropathy (iMN) risk, which provided new insight into potential new targets for the treatment of iMN. However, this relationship remains inconclusive. Our aim was to evaluate the relationship between this polymorphism and iMN susceptibility by performing a meta-analysis. METHODS:Articles were identified in the PubMed, Google Scholar, EMBASE, Cochran Library databases. Meta-analyses were performed for rs2187668 allele frequency, genotypes, and the association with iMN susceptibility. Subgroup analyses, publication bias and sensitivity analyses were also conducted. RESULTS:11 eligible studies (3209 cases and 7358 controls) from 7 articles were included. Statistical analyses were carried out using Stata 12.0, combining data from all the relevant studies. The pooled odds ratios (ORs) regarding the association between the HLA-DQA1 rs2187668 polymorphism and iMN risk were statistically significant [A vs G: OR?=?3.34, 95% confidence interval (CI)?=?2.70-4.13; AA vs GA?+?GG: OR?=?8.69, 95% CI?=?6.64-11.36; GG vs GA?+?AA: OR?=?0.25, 95% CI?=?0.19-0.33;AA vs GG: OR?=?12.61, 95% CI?=?8.02-19.81; GA vs GG: OR?=?3.45, 95% CI?=?2.79-4.25]. CONCLUSIONS:Our pooled analysis showed a significant association between rs2187668-(A) allele and iMN susceptibility, and the intervention of this mutation might bring new therapeutic strategy for iMN. However, further studies should be performed to confirm this finding.
| S-EPMC6221752 | biostudies-literature
Project description:ObjectiveEndometriosis is a common chronic, gynecological disease. Despite many studies on the role of N-acetyltransferase 2 (NAT2) in endometriosis, its clinical significance is unclear. In this study, associations between NAT2 phenotypes as well as single nucleotide polymorphisms (SNPs) within NAT2 (i.e. rs1799929, rs1799930, rs1208, and rs1799931) and endometriosis risk were evaluated using a meta-analysis approach.MethodsEmbase, PubMed, ClinicalTrials.gov, CNKI (China National Knowledge Infrastructure), Wanfang databases, Cochrane Library for clinical trials, and Web of Science were searched to identify relevant articles. ORs (odds ratios) and 95% CIs (95% confidence intervals) were used to estimate the associations between NAT2 polymorphisms and endometriosis risk. Heterogeneity among included studies was also assessed. In addition, a subgroup analysis of NAT2 phenotypes and endometriosis risk based on ethnicity was performed.ResultsNine case-control studies met the inclusion criteria. The odds ratio was 2.30 (95% CI: 1.61-3.28) for the NAT2 slow acetylation phenotype versus the intermediate + fast acetylation phenotype in the Asian population. These results suggest that Asian individuals with the NAT2 slow acetylation phenotype have a 130% increased risk of endometriosis. A significant association was also found for rs1799930 (OR = 0.74; 95% CI, 0.59-0.92), suggesting that individuals with this mutant genotype have a 26% decreased risk of endometriosis.ConclusionsThe rs1799930 mutant genotypes are associated with a decreased risk of endometriosis. No statistically significant associations were found between rs1799931, rs1208, or rs1799929 and endometriosis. Based on a subgroup analysis based on ethnicity, the NAT2 slow acetylation phenotype was found to increase the risk of endometriosis in Asians. No statistically significant associations were found between the NAT2 slow acetylation phenotype and endometriosis risk in Caucasians. Accordingly, NAT2 phenotypes and SNPs are potential biomarkers for the diagnosis and treatment of endometriosis.
| S-EPMC6934289 | biostudies-literature
Project description:BACKGROUND:Murine double minute 2 homolog (MDM2) plays an important role in the downregulation of P53 tumor suppressor gene. MDM2 inhibits P53 transcriptional activity and thereby results in accelerated tumor formation. Overexpression of MDM2 has been found in several cancer types including endometrial cancer. SNP309 is located in the promoter region of MDM2 and contributes to the overexpression of MDM2. The association between MDM2 SNP309 polymorphism and endometrial cancer risk has been investigated in several studies; however, the conclusion remains controversial. OBJECTIVES:We performed the present meta-analysis to give a comprehensive conclusion of the association between MDM2 SNP309 polymorphism and endometrial cancer susceptibility. METHODS:We conducted a literature research on PubMed, Embase, Cochrane Library, OVID, Web of Science, Wan Fang, CNKI, and CQVIP databases up to July 31, 2018. Newcastle-Ottawa scale was used to assess the quality of studies. We evaluated the strength of association by combining odds ratios (ORs) and 95% confidence intervals (CIs) in 5 different genetic models under a fixed-effect model or random-effect model. We further conducted subgroup analysis by ethnicity, source of control, histological type, clinical type, grade, and stage of tumor. Sensitivity analysis and publication bias were also performed. RESULTS:Nine eligible studies were finally included in our meta-analysis. We found MDM2 SNP309 polymorphism increased the risk of endometrial cancer under allele model (OR: 1.23, 95% CI: 1.06-1.41, P?=?.005), homozygote model (OR: 1.43, 95% CI: 1.13-1.81, P?=?.003) and recessive model (OR: 1.55, 95% CI: 1.17-2.04, P?=?.002). Subgroup analysis suggested a similar elevated risk in both Asians and Caucasians. We identified a strong association of enhanced susceptibility to endometrial cancer in endometrioid group (OR: 2.13, 95% CI: 1.28-3.54, P?=?.004) and Type I group (OR: 1.89, 95% CI: 1.25-2.86, P?=?.002) under dominant model. We identified no significant publication bias according to Egger's test. CONCLUSIONS:Our meta-analysis suggested that MDM2 SNP309 polymorphism increased the risk of endometrial cancer significantly, especially in endometrioid and Type I endometrial cancer, indicating MDM2 could serve as a potential diagnostic factor marker for endometrial cancer.
| S-EPMC6310604 | biostudies-other
Project description:AimsIn abdominal aortic aneurysm (AAA), macrophages are detected in the proximity of aortic smooth muscle cells (SMCs). We have previously demonstrated in a murine model of AAA that apoptotic SMCs attract monocytes and other leukocytes by producing MCP-1. Here we tested whether infiltrating macrophages also directly contribute to SMC apoptosis.Methods and resultsUsing a SMC/RAW264.7 macrophage co-culture system, we demonstrated that MCP-1-primed RAWs caused a significantly higher level of apoptosis in SMCs as compared to control macrophages. Next, we detected an enhanced Fas ligand (FasL) mRNA level and membrane FasL protein expression in MCP-1-primed RAWs. Neutralizing FasL blocked SMC apoptosis in the co-culture. In situ proximity ligation assay showed that SMCs exposed to primed macrophages contained higher levels of receptor interacting protein-1 (RIP1)/Caspase 8 containing cell death complexes. Silencing RIP1 conferred apoptosis resistance to SMCs. In the mouse elastase injury model of aneurysm, aneurysm induction increased the level of RIP1/Caspase 8 containing complexes in medial SMCs. Moreover, TUNEL-positive SMCs in aneurysmal tissues were frequently surrounded by CD68(+)/FasL(+) macrophages. Conversely, elastase-treated arteries from MCP-1 knockout mice display a reduction of both macrophage infiltration and FasL expression, which was accompanied by diminished apoptosis of SMCs.ConclusionOur data suggest that MCP-1-primed macrophages are more cytotoxic. MCP-1 appears to modulate macrophage cytotoxicity by increasing the level of membrane bound FasL. Thus, we showed that MCP-1-primed macrophages kill SMCs through a FasL/Fas-Caspase8-RIP1 mediated mechanism.
| S-EPMC3954911 | biostudies-literature