ArticleActa pharmacologica Sinica2021
MicroRNA-17-3p suppresses NF-κB-mediated endothelial inflammation by targeting NIK and IKKβ binding protein.
Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Rare-Earth Nanomaterials for Advanced Theranostics of Atherosclerosis.Chemical & biomedical imaging · 2026Review
- Downregulation of circ_0001112 Enhances Myocardial Infarction Through Regulation of miR-324-5p/CDK6 Axis.Journal of biochemical and molecular toxicology · 2026Article
- Dental pulp stem cell-derived exosomes attenuate psoriatic inflammation by restoring epithelial redox homeostasis via a miR-1246/miR-17-3p-GPX2-NF-κB axis.Stem cell research & therapy · 2026Article
- Differential microRNA expression profiles and predicted miRNA-mRNA regulatory networks in human macrophage-like cells infected with Leishmania infantum.Scientific reports · 2026Article
- Integrated analysis of porcine brain microRNA profiles following pediatric diffuse traumatic brain injury.Acta neuropathologica communications · 2026Article
- Exosomal miRNA expression in transplant recipients with EBV-associated post-transplant lymphoproliferative disorder.Frontiers in immunology · 2026Article
- Comparative study of the effects of baicalin and probenecid on microRNA expression profiles in porcine aortic vascular endothelial cells infected by Glaesserella parasuis.BMC veterinary research · 2025Article
- Dysregulation of lncRNA GATA3-AS1 is Involved in the Pathogenesis of Pulpitis by the Regulation of miR-17-3p.Journal of inflammation research · 2025Article
- MicroRNAs modulation by isodrimeninol fromFrontiers in oral health · 2025Article
- TRAPPopathies: Severe Multisystem Disorders Caused by Variants in Genes of the Transport Protein Particle (TRAPP) Complexes.International journal of molecular sciences · 2024Review
- Curcumin-dependent phenotypic transformation of microglia mediates resistance to pseudorabies-induced encephalitis.Veterinary research · 2023Article
- Identifying MicroRNA Markers That Predict COVID-19 Severity Using Machine Learning Methods.Life (Basel, Switzerland) · 2022Article
- Enhanced Anti-Inflammatory Effects of Silibinin and Capsaicin Combination in Lipopolysaccharide-Induced RAW264.7 Cells by Inhibiting NF-κB and MAPK Activation.Frontiers in chemistry · 2022Article
- Inflammatory Mechanisms Contributing to Endothelial Dysfunction.Biomedicines · 2021Review
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Nuclear factor kappa B (NF-κB) activation contributes to many vascular inflammatory diseases. The present study tested the hypothesis that microRNA-17-3p (miR-17-3p) suppresses the pro-inflammatory responses via NF-κB signaling in vascular endothelium. Human umbilical vein endothelial cells (HUVECs), transfected with or without miR-17-3p agomir/antagomir, were exposed to lipopolysaccharide (LPS), and the inflammatory responses were determined. The cellular target of miR-17-3p was examined with dual-luciferase reporter assay. Mice were treated with miR-17-3p agomir and the degree of LPS-induced inflammation was determined. In HUVECs, LPS caused upregulation of miR-17-3p. Overexpression of miR-17-3p in HUVECs inhibited NIK and IKKβ binding protein (NIBP) protein expression and suppressed LPS-induced phosphorylation of inhibitor of kappa Bα (IκBα) and NF-κB-p65. The reduced NF-κB activity was paralleled by decreased protein levels of NF-κB-target gene products including pro-inflammatory cytokine [interleukin 6], chemokines [interleukin 8 and monocyte chemoattractant protein-1] and adhesion molecules [vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and E-selectin]. Immunostaining revealed that overexpression of miR-17-3p reduced monocyte adhesion to LPS-stimulated endothelial cells. Inhibition of miR-17-3p with antagomir has the opposite effect on LPS-induced inflammatory responses in HUVECs. The anti-inflammatory effect of miR-17-3p was mimicked by NIBP knockdown. In mice treated with LPS, miR-17-3p expression was significantly increased. Systemic administration of miR-17-3p for 3 days suppressed LPS-induced NF-κB activation and monocyte adhesion to endothelium in lung tissues of the mice. In conclusion, miR-17-3p inhibits LPS-induced NF-κB activation in HUVECs by targeting NIBP. The findings therefore suggest that miR-17-3p is a potential therapeutic target/agent in the management of vascular inflammatory diseases.
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