5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Study on the Relationship between lncRNA Gene Polymorphism and Systemic Lupus Erythematosus

      research-article
      1 , 1 , 2 , 1 ,
      Computational and Mathematical Methods in Medicine
      Hindawi

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Systemic lupus erythematosus (SLE) is an autoimmune disease that can cause damage to multiple systems of the body. A number of studies have shown that long-chain noncoding RNA (lncRNA) can participate in the occurrence and development of a variety of autoimmune diseases. This study is aimed at detecting the expression levels of 5 lncRNAs in SLE patients and healthy controls and at exploring the relationship between expression levels and clinical symptoms and laboratory indicators.

          Methods

          The design type of this study is a case-control study. A total of 76 SLE patients and 71 healthy controls were included in the first phase of the study. Real-time fluorescence quantitative polymerase chain reaction was used to detect the expression level of 5 kinds of lncRNAs including lnc7514, lnc0640, lncagf, nc3643, and lnc5150 in PBMCs of two groups of patients; the expression of lncRNAs in the case group and the control group was analyzed. We analyzed the differences in the expression levels of lncRNAs between case and control groups, and explored the association of expression levels with clinical manifestations and laboratory characteristics. SPSS23.0 was used to analyze the expression level and gene polymorphism results; the statistical analysis test level α = 0.05.

          Results

          The expression level of lnc0640 in PBMCs of SLE patient group was higher than that of healthy control group ( Z = −3.56, P = 0.03). However, lnc5150 was lower than in healthy controls ( Z = −7.16, P < 0.001). lnc3643 expression levels were lower in SLE patients of SLE patients with pleurisy was lower than that of patients without pleurisy ( Z = −2.44, P = 0.02). Low lnc3643 expression levels were observed in PBMCs with SLE patients with rash symptoms ( Z = −2.75, P = 0.013). SLE expressed lower lnc3643 levels in PBMCs with SLE compared with those without pleurisy ( Z = −2.42, P = 0.02). The above differences were statistically significant. Association analysis of lncRNA expression levels and clinical manifestations in SLE patients found that SLE was lower than those without rash or pleurisy (both P < 0.05); association analysis of lncRNA expression level and laboratory results found a negative correlation between lnc3643, lnc7514, and SLE disease activity score (SLEDAI-2K), blood sink (ESR), and C-reactive protein (CRP) (all P < 0.05).

          Conclusions

          lnc0640 was overexpressed in PBMCs in SLE patients compared with healthy controls. lnc3643 was negatively correlated with SLEDAI, and expression levels were associated with SLE patients with arthritis, rash, and pleuritis.

          Related collections

          Most cited references18

          • Record: found
          • Abstract: found
          • Article: not found

          Novel paradigms in systemic lupus erythematosus

          The heterogeneity of systemic lupus erythematosus (SLE), long recognised by clinicians, is now challenging the entire lupus community, from geneticists to clinical investigators. Although the outlook for patients with SLE has greatly improved, many unmet needs remain, chief of which is the development of safer and more efficacious therapies. To develop innovative therapies, a far better understanding of SLE pathogenesis as it relates to the array of clinical phenotypes is needed. Additionally, to efficiently achieve these goals, the lupus community needs to refine existing clinical research tools and better adapt them to overcome the obstacles created by the heterogeneity of manifestations. Here, we review progress towards the ultimate goal of safely reducing disease activity and preventing damage accrual and death. We discuss the new classification criteria from the European League Against Rheumatism and American College of Rheumatology, novel definitions of remission and low lupus disease activity, and new proposals for the histological classification of lupus nephritis. Recommendations for the treatment of SLE and novel approaches to drug development hold much promise to further enhance SLE outcomes.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Mapping Systemic Lupus Erythematosus heterogeneity at the single-cell level

            Patients with Systemic Lupus Erythematosus (SLE) display a complex blood transcriptome whose cellular origin is poorly resolved. Using single-cell RNA-seq, we profiled ~276,000 PBMCs from 33 children with SLE (cSLE) with different degrees of disease activity (DA) and 11 matched controls. Increased expression of interferon-stimulated genes (ISGs) distinguished cSLE from healthy control cells. The high-ISG expression signature (ISGhi) derived from a small number of transcriptionally defined subpopulations within major cell types, including monocytes, CD4+ and CD8+ T cells, natural killer cells, conventional dendritic cells (cDCs), plasmacytoid DCs (pDCs), B cells and especially plasma cells. Expansion of unique subpopulations enriched in ISGs and/or in monogenic lupus-associated genes classified patients with the highest DA. Profiling of ~82,000 single peripheral blood mononuclear cells (PBMCs) from adult SLE patients confirmed the expansion of similar subpopulations in patients with the highest DA. This study lays the groundwork for resolving the origin of the SLE transcriptional signatures and the disease heterogeneity towards precision medicine applications.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found

              Complement genes contribute sex-biased vulnerability in diverse illnesses

              Many common illnesses differentially affect men and women for unknown reasons. The autoimmune diseases lupus and Sjögren’s syndrome affect nine times more women than men 1 , whereas schizophrenia affects men more frequently and severely 2 . All three illnesses have their strongest common genetic associations in the Major Histocompatibility Complex (MHC) locus, an association that in lupus and Sjögren’s syndrome has long been thought to arise from alleles of the human leukocyte antigen (HLA) genes at that locus 3–6 . Here we show that the complement component 4 (C4) genes, which are also in the MHC locus and were recently found to increase risk for schizophrenia 7 , generate 7-fold variation in risk for lupus (95% CI: 5.88–8.61; p < 10−117 in total) and 16-fold variation in risk for Sjögren’s syndrome (95% CI: 8.59–30.89; p < 10−23 in total) among individuals with common C4 genotypes, with C4A protecting more strongly than C4B in both illnesses. The same alleles that increase risk for schizophrenia greatly reduced risk for lupus and Sjögren’s syndrome. In all three illnesses, C4 alleles acted more strongly in men than in women: common combinations of C4A and C4B generated 14-fold variation in risk for lupus, 31-fold variation in risk for Sjögren’s syndrome, and 1.7-fold variation in schizophrenia risk among men (vs. 6-fold, 15-fold, and 1.26-fold among women respectively). At a protein level, both C4 and its effector C3 were present at greater levels in men than women in cerebrospinal fluid (p < 10−5 for both C4 and C3) and plasma 8,9 among adults ages 20–50, corresponding to the ages of differential disease vulnerability. Sex differences in complement protein levels may help explain the larger effects of C4 alleles in men, women’s greater risk of SLE and Sjögren’s, and men’s greater vulnerability in schizophrenia. These results implicate the complement system as a source of sexual dimorphism in vulnerability to diverse illnesses.
                Bookmark

                Author and article information

                Contributors
                Journal
                Comput Math Methods Med
                Comput Math Methods Med
                cmmm
                Computational and Mathematical Methods in Medicine
                Hindawi
                1748-670X
                1748-6718
                2022
                27 February 2022
                : 2022
                : 4446016
                Affiliations
                1Clinical Laboratory, First Affiliated Hospital of Harbin Medical University, 150001, China
                2Clinical Laboratory, Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), 266033, China
                Author notes

                Academic Editor: Min Tang

                Author information
                https://orcid.org/0000-0002-2508-2853
                Article
                10.1155/2022/4446016
                8898853
                35265170
                4f80d341-0b73-4cec-be50-4fdac5dd65c7
                Copyright © 2022 Xue Guan et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 31 December 2021
                : 7 January 2022
                : 11 January 2022
                Categories
                Research Article

                Applied mathematics
                Applied mathematics

                Comments

                Comment on this article