Systemic lupus erythematosus (SLE) is an autoimmune disease, with multiple genetic and environmental factors involving in its etiology. Angiotensin converting enzyme (ACE) gene was reported to have important roles in the development and progression of SLE. In this study, a case-control study was carried out to investigate the effects of seven SNPs and I/D in ACE gene in the development of SLE in Northern China. Seven SNPs including A5466C, T3892C, A240T, C1237T, G2215A, A2350G and C3409T were genotyped by PCR-RFLP method, and I/D was examined by agarose gel electrophoresis followed PCR directly. 314 SLE patients were compared to 320 normal controls in the study. Data were analyzed by SPSS 13.0 and HaploView software. The frequency distribution of SNP A2350G and Alu I/D and five haplotypes (AAAACCCI, AGAACCTD, AAAATCTI, TAAATTTI and TAAATCTI) were demonstrated to be different between case and control groups significantly. Whereas other SNPs and haplotypes had no differences in two cohorts. The results revealed that variations of ACE gene had association with SLE, which indicated ACE gene may play an important role in pathogenesis of SLE in Northern Chinese Han population.
PurposeThe association between CD14 -159C/T polymorphism and the susceptibility to gastric cancer (GC) has been reported. However, the results were inconclusive. In the present study, a case–control study and a meta-analysis were performed to assess the possible association between -159C/T in the CD14 gene and GC risk.Patients and methodsRelevant studies were searched in several databases including PubMed, Web of Science, EMBASE, Chinese National Knowledge Infrastructure database, and Wanfang database (last search was performed on December 30, 2015). In addition, a case–control study involving 164 GC cases and 169 controls was also performed in the analysis. Statistical analysis was performed by the software Revman5.3.ResultsA total of ten published studies and the present case–control study involving 2,844 GC and 3,983 controls were included for the meta-analysis. The analysis result indicated that the T allele of CD14 -159C/T polymorphism did not confer risk for GC (in our study: [P=0.93]; in the meta-analysis: T vs 2N odds ratio =1.28 and 95% confidence interval (CI) =0.95–1.24, [P=0.24]). However, we found a significant association in the recessive model (in our study: TT vs TC+CC [P=0.04]; in the meta-analysis: TT vs TC+CC odds ratio =1.12 and 95% CI =1.01–1.26, [P=0.04]). Furthermore, a subgroup analysis by ethnicity showed that TT genotype was significantly associated with GC in Asian (odds ratio =1.17 and 95% CI =1.02–1.34, [P=0.02]) but not in Caucasian.ConclusionOur results highlight the TT genotype of CD14 -159C/T as a genetic susceptibility factor for gastric cancer, particularly, in Asians and population-based controls.
Interleukin- (IL-) 33 contributes to various inflammatory processes. IL-33/ST2 activation participates in systemic lupus erythematous via binding to the receptor of Suppression of Tumorigenicity 2 protein (ST2). However, whether IL-33/ST2 interferes with the nosogenesis of cutaneous lupus erythematosus (CLE) has not been reported so far. Herein, we proposed to disclose the impacts on IL-33/ST2 activation and Ro60 on CLE and their potential implications in the photosensitization of CLE cells. IL-33, ST2, and Ro60 in CLE patients’ skin lesions were detected. Murine keratinocytes stimulated with or without IL-33 were irradiated by ultraviolet B (UVB), and the levels of Ro60 and inflammation markers were determined. Keratinocytes were cocultured with J774.2 macrophages and stimulated with IL-33 for analysis of chemostasis. The results identified that IL-33, ST2, and downstream inflammation markers were significantly upregulated in CLE lesions with Ro60 overexpression. Additionally, IL-33 treatment promoted the upregulation of Ro60 induced by UVB treatment in murine keratinocytes. Moreover, IL-33 stimulates keratinocytes to induce macrophage migration via enhancing the generation of the chemokine (C–C motif) ligands 17 and 22. Meanwhile, the silencing of ST2 or nuclear factor-kappa B (NF-κB) suppression abolished IL-33-induced upregulation of Ro60 in keratinocytes. Similarly, the inhibition of SOX17 expression was followed by downregulation of Ro60 in keratinocytes following IL-33 stimulation. In addition, UVB irradiation upregulated SOX17 in keratinocytes. Conclusively, the IL-33/ST2 axis interferes with Ro60-regulated photosensitization via activating the NF-κB- and PI3K/Akt- and SOX17-related pathways.
Objective. From the pathogenic mechanism point of view, systemic lupus erythematosus (SLE) features prominently in T lymphocyte apoptosis. Yet the regulatory mechanism underlying SLE cell apoptosis remains to be explored. This research intends to clarify the role played by miR-137 in SLE and the underlying mechanisms. Methods. Twenty SLE patients (SLE group) and twenty healthy controls (control group) were selected, from whom peripheral blood CD4+ T cells were isolated via magnetic-activated cell sorting. Reverse transcription-polymerase chain reaction (RT-PCR) quantified miR-137 and AMP-activated protein kinase (AMPK) in CD4+ T cells. Further, transfection of miR-137 mimics and inhibitors into CD4+ T cells was carried out to alter miR levels. Levels of pyroptosis, apoptosis, and inflammatory- and pyroptosis-related proteins were determined through PI staining, flow cytometry, and Western blotting, respectively. A luciferase reporter gene assay identified the targeting relation between miR-137 and AMPK. Results. SLE patients showed downregulated miR-137 and upregulated AMPK in CD4+ T cells than controls. miR-137 upregulation by miR-137 mimic transfection inhibited Jurkat cell pyroptosis and apoptosis at both mRNA and protein levels and suppressed NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome activity and pyroptosis-related protein gasdermin D (GSDMD), while miR-137 inhibitor transfection contributed to completely opposite effects. miR-137 directly targeted AMPK, as indicated by the luciferase reporter gene assay. Furthermore, miR-137 inhibitor intervention induced healthy CD4+ T cell pyroptosis and apoptosis via mediating AMPK, whereas miR-137 mimic transfection into CD4+ T cells of SLE patients leads to opposite results. Conclusion. Upregulating miR-137 inhibits CD4+ T cell pyroptosis in SLE patients by modulating the AMPK pathway, suggesting the potential diagnostic and therapeutic role of miR-137 in SLE.
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