ArticleOpen medicine (Warsaw, Poland)2020
NEAT1 Promotes LPS-induced Inflammatory Injury in Macrophages by Regulating MiR-17-5p/TLR4.
Article in Open medicine (Warsaw, Poland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Neuroepigenetic regulation by long non-coding RNAs in sepsis-associated encephalopathy: cell-type programs and translational biomarkers.Neurogenetics · 2026Review
- Oxidative stress-driven epigenetic reprogramming of immune cells in COPD: from epitranscriptomic and metabolic crosstalk to treatable traits.Frontiers in immunology · 2026Review
- miR-17-5p: bridging the gap between disease mechanisms and therapeutic innovations.Epigenomics · 2025Review
- Distinct expression of NEAT1 isoforms in Parkinson's disease models suggests different roles of the variants during the disease course.Scientific reports · 2025Article
- Single-nucleus transcriptomics reveals sepsis-related neurovascular dysfunction in the human hippocampus.Frontiers in immunology · 2025Article
- Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Cell-type brain-region specific changes in prefrontal cortex of a mouse model of alcohol dependence.Neurobiology of disease · 2024Article
- Role of Macrophage lncRNAs in Mediating Inflammatory Processes in Atherosclerosis and Sepsis.Biomedicines · 2023Review
- Potential regulatory effects of stem cell exosomes on inflammatory response in ischemic stroke treatment.World journal of stem cells · 2023Review
- Identification of potential biomarkers and pathways for sepsis using RNA sequencing technology and bioinformatic analysis.Heliyon · 2023Article
- Inflammatory MicroRNAs and the Pathophysiology of Endometriosis and Atherosclerosis: Common Pathways and Future Directions Towards Elucidating the Relationship.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- METTL3-mediated macrophage exosomal NEAT1 contributes to hepatic fibrosis progression through Sp1/TGF-β1/Smad signaling pathway.Cell death discovery · 2022Article
- Urinary microRNAome in healthy cats and cats with pyelonephritis or other urological conditions.PloS one · 2022Article
- Assessing the suitability of long non-coding RNAs as therapeutic targets and biomarkers in SARS-CoV-2 infection.Frontiers in molecular biosciences · 2022Review
- Article
- Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation.Journal of inflammation research · 2022Review
- Microglia Polarization: A Novel Target of Exosome for Stroke Treatment.Frontiers in cell and developmental biology · 2022Review
- Association Between Genetic Polymorphisms of lncRNAInfection and drug resistance · 2022Article
- Long non-coding RNA NEAT1 contributes to lipopolysaccharide-induced inflammation and apoptosis of human middle ear epithelial cells via regulating the miR-301b-3p/TLR4 axis.Experimental and therapeutic medicine · 2021Article
- CircTLK1 modulates sepsis-induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis-mediated mitochondrial DNA damage by sponging miR-17-5p.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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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
backgroundThe inflammatory response of macrophages is responsible for sepsis. Long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to be involved in sepsis development. However, its underlying mechanism remains largely unclear. This study aims to investigate the effect of NEAT1 on inflammatory response of macrophages and explore the regulatory network of NEAT1/microRNA-17-5p (miR-17-5p)/Toll-like receptor 4 (TLR4).
methodsThe serum samples of 68 sepsis patients and 32 heathy controls were collected. THP-1 macrophages were treated with lipopolysaccharide (LPS) to induce inflammatory injury model of sepsis. The expressions of NEAT1, miR-17-5p and TLR4 were measured by quantitative real-time polymerase chain reaction or western blot. The inflammatory response was investigated by levels of inflammatory cytokines, tumor necrosis factor-alpha (TNF-ɑ), interleukin-1beta (IL-1β) and IL-6 as well as nitric oxide (NO) production. The interaction among NEAT1, miR-17-5p and TLR4 were investigated by bioinformatics analysis, luciferase reporter assay and RNA pull-down.
resultsNEAT1 expression was enhanced in patient serum and associated with severity of sepsis. Knockdown of NEAT1 inhibited levels of TNF-ɑ, IL-1β, IL-6 and NO release in LPS-treated macrophages. miR-17-5p is bound to NEAT1 and its abrogation reversed NEAT1 knockdown-mediated inhibition of inflammatory response in LPS-treated macrophages. Overexpression of miR-17-5p weakened LPS-induced inflammatory response. TLR4 as a target of miR-17-5p was regulated by NEAT1 and miR-17-5p. TLR4 res-to ration alleviated silencing NEAT1-induced inflammatory suppression.
conclusionSilence of NEAT1 suppressed LPS-induced inflammatory response of macrophages by mediating miR-17-5p and TLR4, indicating that NEAT1 might be a promising target for sepsis treatment.
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