Similar Datasets
Project description:CircRNAs are novel non-coding RNAs which can serve as microRNA sponge and regulate gene transcription through promoting expression of their parent genes or competing with splicing of their parent genes. Moveover, there is increasing evidence showing that aberrant expressions of circRNAs are implicated in various cancers. Yet, their roles in systemic lupus erythematosus (SLE), a prototypical autoimmune disease, remain unknown. To reveal the implications of circRNAs in SLE, we used Human circRNA Array v2.0 microarrays to measure the expression profiles of circRNAs in T cells of patients with SLE and healthy controls. We found 129 differentially expressed circRNAs (fold change >2; P <0.05) in SLE patients compared with controls. Home-made computer program based on TargetScan and miRanda was applied to predict miRNA targets of circRNAs and identify 5 miRNAs with the highest mirSVR score for each circRNA.Downregulation of circRNA hsa_circ_0045272 was established using Real-time quantitative PCR. These results showed abrrant expression profiles of circRNAs in T cells of SLE patients and revealed their potential role in SLE.
2018-07-17 | GSE84655 | GEO
Project description:long non-coding RNAs (lncRNAs) are novel non-coding RNAs which play an important part in regulating gene transcription and translation, modulating protein function, and acting as competing endogeneous RNA. Moveover, there is increasing evidence showing that aberrant expressions of lncRNAs are implicated in various cancers. Yet, their roles in systemic lupus erythematosus (SLE), a prototypical autoimmune disease, remain unknown. To reveal the implications of LncRNAs in SLE, we used Human LncRNA Array v3.0 microarrays to measure the expression profiles of lncRNAs in T cells of patients with SLE and healthy controls. we found 869 upregulated lncRNAs and 1066 downregulated lncRNAs in SLE patients compared with controls. Coding-non-coding gene coexpression (CNC) network was constructed based on the correlation analysis between the differentially expressed lncRNA and mRNA. Downregulation of two lncRNAs, uc001ykl.1 and ENST00000448942 was established using Real-time quantitative PCR. These results showed abrrant expression profiles of lncRNAs in T cells of SLE patients and revealed their potential role in SLE.
2018-03-08 | GSE84654 | GEO
Project description:Comprehensive expression profiling reveals the potential role of lncRNAs and circRNAs in systemic lupus erythematosus
| PRJNA330775 | ENA
Project description:Background:Long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs)are involved in the progression of discoid lupus erythematosus (DLE), but an understanding of their underlying mechanisms remains elusive. To explore the expression profiles of lncRNAs and circRNAs in DLE, we surveyed the lncRNA/circRNA and mRNA expression profiles in the epithelia of oral DLE and adjacent normal tissues. Methods:The lesional and non-lesional lower lips of three DLE patients were analysed by RNA-sequencing (RNA-seq). The principal functions of the significantly deregulated genes were identified using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. And the correlated expression networks (coding-noncoding co-expression and lncRNAs-transcription factor-mRNA) were evaluated as well. Results:Hundreds of significantly changed lncRNAs and mRNAs and dozens of significantly changed circRNAs were identified. lncRNA lnc-MIPOL1-6 and IncRNA IncDDX47-3 expressions were correlated with immune response-related genes, including IL19, CXCL1, CXCL11, and TNFSF15. Up-regulated IncRNA-TF network consists of 8 TFs and 74 related lncRNAs. The lncRNA-TF-gene trans-regulation consisting of 204 lncRNAs,39 TFs, and correlated 3 genes. Conclusions:These results demonstrate that lncRNAs and circRNAs can influence the progression of DLE. Certain mRNAs/lncRNAs/circRNAs may have substantial value in DLE diagnosis and therapy.
| S-EPMC6990042 | biostudies-literature
Project description:Our understanding of the genetic basis of systemic lupus erythematosus has progressed rapidly in recent years. While many genetic polymorphisms have been associated with disease susceptibility, the next major step involves integrating these genetic polymorphisms into the molecular mechanisms and cellular immunology of the human disease. In this review, we summarize some recent work in this area, including the genetics of the type I IFN response in SLE, including polygenic and monogenic factors, as well as epigenetic influences. Contributions of both HLA and non-HLA polymorphisms to the complex genetics of SLE are reviewed. We also review recent reports of specific gene deficits leading to monogenic SLE-like syndromes. The molecular functions of common SLE-risk variants are reviewed in depth, including regulatory variations in promoter and enhancer elements and coding-change polymorphisms, and studies which are beginning to define the molecular and cellular functions of these polymorphisms in the immune system. We discuss epigenetic influences on lupus, with an emphasis on micro-RNA expression and binding, as well as epigenetic modifications that regulate the expression levels of various genes involved in SLE pathogenesis and the ways epigenetic marks modify SLE susceptibility genes. The work summarized in this review provides a fascinating window into the biology and molecular mechanisms of human SLE. Understanding the functional mechanisms of causal genetic variants underlying the human disease greatly facilitates our ability to translate genetic associations toward personalized care, and may identify new therapeutic targets relevant to human SLE disease mechanisms.
| S-EPMC4628859 | biostudies-literature
Project description:Systemic lupus erythematosus (SLE) is a challenging disease caused by both genetic and environmental influences. Symptoms of SLE vary and they may come and go, therefore diagnosis and treatment of the disease is difficult. Serum metabolites can not only serve as biomarkers of the disease but also can reveal the pathogenesis. Thus, it is important to find reliable biomarkers for early diagnosis and treatment of the disease, which would greatly benefit SLE patients. Our purpose was to study the metabolite profiles in active systemic lupus erythematosus and to identify metabolites that are significantly altered. Serum samples from 34 participants (17 SLE and 17 healthy) were collected and analyzed. Untargeted lipidomics and metabolomics were used to study the metabolite profiles in serum by high-performance liquid chromatography-tandem mass spectrometry. Serum enzyme-linked immunosorbent assay was performed to validate differentially expressed metabolites. We identified differential expression of over 50 metabolites. These metabolites include several new SLE related metabolite species such as ceramide, trimethylamine N-oxide, xanthine, which were significantly elevated in the serum of active systemic lupus erythematosus patients. Some other metabolites include acylcarnitine, caffeine, hydrocortisone, itaconic acid and serotonin were down-regulated. Our study characterizes the circulating metabolites in active systemic lupus erythematosus and provides several candidate biomarkers for the diagnosis and potential therapeutic targets of the disease.
| S-EPMC6945160 | biostudies-literature
Project description:Systemic lupus erythematosus (SLE) is a multisystemic disease, caused by a variety of factors, which lead to immunological abnormalities. Osteopontin (OPN) is a pleiotropic protein, important in bone remodeling and immune system signaling. OPN, produced by various cells, including immune cells, plays a key role in regulating T-helper 1/T-helper 2 balance, stimulating B lymphocytes to produce antibodies, regulating macrophages, neutrophils and inducing dendritic cells. OPN expression is influenced by genetic polymorphisms of its promoter, hormones and cytokines. Over expression of OPN has been associated with the pathogenesis of immune-mediated diseases. OPN has been implicated in the development of murine model of lupus and in humans with SLE. In this review, I will present current state of research on the role of OPN and OPN gene polymorphisms in pathogenesis and clinical course of SLE. A better understanding of the role of OPN in SLE will contribute to more precise diagnosis and treatment of the disease.
| S-EPMC4244532 | biostudies-literature
Project description:Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease characterized by the production of various autoantibodies and deposition of immune complexes. SLE is a heterogenous disease, and the pattern of organ involvement and response to treatment differs significantly among patients. Novel biological markers are necessary to assess the extent of organ involvement and predict treatment response in SLE. Lysophosphatidic acid is a lysophospholipid involved in various biological processes, and autotaxin (ATX), which catalyzes the production of lysophosphatidic acid in the extracellular space, has gained attention in various diseases as a potential biomarker. The concentration of ATX is increased in the serum and urine of patients with SLE and lupus nephritis. Recent evidence suggests that ATX produced by plasmacytoid dendritic cells may play an important role in the immune system and pathogenesis of SLE. Furthermore, the production of ATX is associated with type I interferons, a key cytokine in SLE pathogenesis, and ATX may be a potential biomarker and key molecule in SLE.
| S-EPMC10130763 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-06-03 | E-GEOD-46923 | biostudies-arrayexpress
Project description:MicroRNAs control the differentiation and function of B cells, which are considered key elements in the pathogenesis of systemic lupus erythematosus (SLE). However, a common micro(mi)RNA signature has not emerged since published data includes patients of variable ethnic background, type of disease, and organ involvement, as well as heterogeneous cell populations. Here, we aimed at identifying a miRNA signature of purified B cells from renal and non-renal severe SLE patients of Latin American background, a population known to express severe disease. Genome-wide miRNA expression analyses were performed on naive and memory B cells and revealed two categories of miRNA signatures. The first signature represents B cell subset-specific miRNAs deregulated in SLE: 11 and six miRNAs discriminating naive and memory B cells of SLE patients from healthy controls (HC), respectively. Whether the miRNA was up or down-regulated in memory B cells as compared with naive B cells in HC, this difference was abolished in SLE patients, and vice versa. The second signature identifies six miRNAs associated with specific pathologic features affecting renal outcome, providing a further understanding for SLE pathogenesis. Overall, the present work provided promising biomarkers in molecular diagnostics for disease severity as well as potential new targets for therapeutic intervention in SLE.
| S-EPMC4581178 | biostudies-literature