ArticleFrontiers in immunology2019
Excessive miR-152-3p Results in Increased BAFF Expression in SLE B-Cells by Inhibiting the KLF5 Expression.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Epigenetic regulation of B cell tolerance and dysfunction in autoimmune disease.Nature reviews. Immunology · 2026Review
- LncRNA GAS6-AS1 affects doxorubicin‑induced cardiomyocyte injury in H9c2 cells by regulating miR‑152‑3p: a cellular model relevant to heart failure.Journal of cardiothoracic surgery · 2026Article
- Epigenetic Alterations in Microbiome-Host Interactions in Inflammatory and Autoimmune Diseases.International journal of molecular sciences · 2026Review
- MicroRNAs in immune-related diseases: mechanism, functions and therapeutic perspectives.Frontiers in immunology · 2026Review
- Basophil-derived exosomes exacerbate systemic lupus erythematosus by regulating B-cell proliferation via miR-24550.BMC medicine · 2025Article
- Extracellular Vesicle-Derived miRNAs in Ischemic Stroke: Roles in Neuroprotection, Tissue Regeneration, and Biomarker Potential.Cellular and molecular neurobiology · 2025Review
- Role of miRNAs in Apoptosis Pathways of Immune Cells in Systemic Lupus Erythematosus.Immunity, inflammation and disease · 2025Review
- KLF5 Regulation of Exosome-Derived miR-152-3p From Bone Marrow Stem Cells Improves Ventricular Arrhythmia After Myocardial Infarction.Stem cells international · 2025Article
- 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
- MicroRNAs as Key Regulators in RA and SLE: Insights into Biological Functions.Current pharmaceutical design · 2024Review
- Review
- Dysregulated MicroRNAs in the Pathogenesis of Systemic Lupus Erythematosus: A Comprehensive Review.International journal of biological sciences · 2023Review
- Mesenchymal Stem Cells and MSCs-Derived Extracellular Vesicles in Infectious Diseases: From Basic Research to Clinical Practice.Bioengineering (Basel, Switzerland) · 2022Review
- Deficiency of p53 Causes the Inadequate Expression of miR-1246 in B Cells of Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- A time to heal: microRNA and circadian dynamics in cutaneous wound repair.Clinical science (London, England : 1979) · 2022Review
- The emerging role non-coding RNAs in B cell-related disorders.Cancer cell international · 2022Review
- Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022Review
- An update on epigenetic regulation in autoimmune diseases.Journal of translational autoimmunity · 2022Article
- Novel insight into miRNA biology and its role in the pathogenesis of systemic lupus erythematosus.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The increased BAFF expression in B-cells of patients with systemic lupus erythematosus (SLE) is associated with B-cell hyperstimulation and T-cell hyperactivity, but the underlying mechanisms are still unclear. This study aimed to uncover the mechanisms that regulate the BAFF expression in SLE B-cells. The results demonstrated that the expression of miR-152-3p was significantly increased in SLE B-cells compared with normal controls. This study confirmed that Kruppel-like factor 5 (KLF5) was a direct target of miR-152-3p, and it could bind to the promoter region of BAFF and inhibit its expression in B-cells. The upregulation of miRNA-152-3p expression decreased the KLF5 expression and increased the BAFF expression in SLE B-cells. Knockdown of miR-152-3p expression inhibited the self-reactivity of SLE B-cells, thereby reducing the autoantibody production. The increased miR-152-3p expression in SLE B-cells led to an increase in BAFF expression by inhibiting KLF5 expression. These factors caused B-cell self-reactivity and autoantibody production, allowing participation in the disease process of SLE.
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