ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2020
MALAT1 is involved in type I IFNs-mediated systemic lupus erythematosus by up-regulating OAS2, OAS3, and OASL.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.
- The role of microRNAs and long non-coding RNAs in epigenetic regulation of T cells: implications for autoimmunity.Frontiers in immunology · 2025Pooled it
- Pooled it
- The Multi-Omics Landscape of Enzymatic Alterations in Systemic Lupus Erythematosus.Proteomics. Clinical applications · 2026Article
- DTX3L promotes ovarian cancer progression and cisplatin resistance by activating JAK1/STAT1/OAS3 pathway.Scientific reports · 2026Article
- Hypomethylation of the HumanArchives of Iranian medicine · 2026Article
- Identification of Genetic Diagnostic Markers for Systemic Lupus Erythematosus.Genetics research · 2026Article
- Integrated proteomic and transcriptomic profiles reveals the role of OAS3 in dermatomyositis pathogenesis.Frontiers in immunology · 2026Article
- Effect of OASL on oxaliplatin-induced immunogenic cell death in gastric cancer via the cGAS-STING signaling pathway.Cell death discovery · 2025Article
- Comprehensive Analysis of lncRNA/circRNAs-miRNA-mRNA Networks of Oral Lichen Planus.Journal of inflammation research · 2025Article
- Identification and immunoassay of biomarkers associated with T cell exhaustion in systemic lupus erythematosus.Frontiers in immunology · 2025Article
- Importance of Studying Non-Coding RNA in Children and Adolescents with Type 1 Diabetes.Biomedicines · 2024Review
- Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk.Molecular medicine (Cambridge, Mass.) · 2024Article
- RNA-Seq of an LPS-Induced Inflammation Model Reveals Transcriptional Profile Patterns of Inflammatory Processes.Life (Basel, Switzerland) · 2024Article
- Identification of diagnostic model in heart failure with myocardial fibrosis and conduction block by integrated gene co-expression network analysis.BMC medical genomics · 2024Article
- Epigenetic Dysregulation in the Pathogenesis of Systemic Lupus Erythematosus.International journal of molecular sciences · 2024Review
- An updated review on abnormal epigenetic modifications in the pathogenesis of systemic lupus erythematosus.Frontiers in immunology · 2024Review
- Identification of a shared gene signature and biological mechanism between diabetic foot ulcers and cutaneous lupus erythemnatosus by transcriptomic analysis.Frontiers in physiology · 2024Article
- Emerging Role of LncRNAs in Autoimmune Lupus.Inflammation · 2022Review
- Genotype Triad forDiagnostics (Basel, Switzerland) · 2022Article
- Overexpression of OASL upregulates TET1 to induce aberrant activation of CD4Arthritis research & therapy · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease associated with an aberrant activation of immune cells partly due to the dysfunction of cytokines such as type I interferons (IFNs). Long non-coding RNA MALAT1 has been found to play a pathogenic role in SLE; however, the underlying mechanisms are still poorly understood. Bioinformatics analysis showed the up-regulation of type I IFN downstream effectors OAS2, OAS3, and OASL (OAS-like) in CD4+ T cells, CD19+ B cells, and CD33+ myeloid cells in patients with active SLE compared to healthy participants. In this study, peripheral blood mononuclear cells (PBMCs), CD19+ B, and CD4+ T cells were isolated from active SLE patients and healthy participants. PCR was performed to quantify MALAT1, OAS2, OAS3, and OASL expression in immune cells. MALAT1, OAS2, OAS3, and OASL were knocked down in CD4+ T cells to investigate the regulatory effect of MALAT1 on the effectors and their involvement in type I IFNs-mediated inflammation. Results showed higher OAS2, OAS3, and OASL expression in active SLE patients. MALAT1 expression was positively correlated to OAS2, OAS3, and OASL expression in CD19+ B or CD4+ T cells. MALAT1 knockdown decreased OAS2, OAS3, and OASL expression. Treatment with IFN-α-2a increased the expression of TNF-α, IL-1β, and IFN-α in CD4+ T cells. However, knockdown of MALAT1, OAS2, OAS3, and OASL alone inhibited the effect of IFN-α-2a on TNF-α and IL-1β. This study suggested the involvement of MALAT1 in type I IFNs-mediated SLE by up-regulating OAS2, OAS3, and OASL.
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