ArticleAmerican journal of translational research2019
Long non-coding RNA NEAT1/miR-193a-3p regulates LPS-induced apoptosis and inflammatory injury in WI-38 cells through TLR4/NF-κB signaling.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- The Impact of NEAT1 on Inflammatory Responses and Processes in Arthropathic Diseases: Latest Findings and Perspectives.Biochemical genetics · 2026Review
- Comparative Effects ofInternational journal of molecular sciences · 2026Article
- Long noncoding RNAs in ubiquitination, protein degradation, and human diseases.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024Review
- Long Non-coding RNA NEAT1 , NOD-Like Receptor Family Protein 3 Inflammasome, and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2024Article
- METTL3 aggravates cell damage induced by Streptococcus pneumoniae via the NEAT1/CTCF/MUC19 axis.The Kaohsiung journal of medical sciences · 2024Article
- Circular RNA CircDHRS3 Aggravates IL-1β-induced ECM Degradation, Apoptosis, and Inflammatory Response via Mediating MECP2 Expression.Inflammation · 2023Article
- Exosomal Lnc NEAT1 from endothelial cells promote bone regeneration by regulating macrophage polarization via DDX3X/NLRP3 axis.Journal of nanobiotechnology · 2023Article
- miR-193a-3p increases glycolysis under hypoxia by facilitating Akt phosphorylation and PFKFB3 activation in human macrophages.Cellular and molecular life sciences : CMLS · 2022Article
- Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation.Journal of inflammation research · 2022Review
- 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
- Article
- LncRNA NEAT1 Knockdown Alleviates Lipopolysaccharide-Induced Acute Lung Injury by Modulation of miR-182-5p/WISP1 Axis.Biochemical genetics · 2021Article
- Silencing of long non-coding RNA KCNQ1OT1 alleviates LPS-induced lung injury by regulating the miR-370-3p/FOXM1 axis in childhood pneumonia.BMC pulmonary medicine · 2021Article
- LncRNA RP11-248E9.5 and RP11-456D7.1 are Valuable for the Diagnosis of Childhood Pneumonia.International journal of general medicine · 2021Article
- Article
- Autophagy-Associated lncRNAs: Promising Targets for Neurological Disease Diagnosis and Therapy.Neural plasticity · 2020Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pneumonia is a primary pulmonary infection disease with a high morbidity and mortality worldwide. Identification of key long non-coding RNAs (lncRNAs) facilitates to the development of effective therapeutic targets for pneumonia. LncRNA NEAT1 was vital and functional in inflammatory diseases but has not been studied in pneumonia. The aim of this study was to investigate the role of NEAT1 in pneumonia and explore its potential mechanism. Lipopolysaccharide (LPS) was applied into WI-38 cells to establish cell model of pneumonia. Cells were transfected with shRNA-NEAT1, miR-193a-3p or negative control. Real time quantitative PCR and western blot were performed to detect mRNA level and protein expression, respectively. Cell counting kit-8 (CCK-8) assay was performed to detect cell viability. Flow cytometry analysis was performed to determine cell apoptosis. Cell viability was significantly declined and cell apoptosis was increased in LPS-treated WI-38 cells. NEAT1 was upregulated under LPS treatment and NEAT1 inhibition significantly improved cell viability, decreased cell apoptosis and the production of inflammatory cytokines. The expression level of miR-193a-3p was regulated by NEAT1, and NEAT1 reversed miR-193a-3p overexpression-alleviated inflammatory injury that include inflammation and apoptosis induced by LPS. Further, NEAT1 and miR-193a-3p regulated the activity of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling. Therefore, NEAT1 may function as a ceRNA by sponging miR-193a-3p to regulate the activation of TLR4/NF-κB signaling to alleviate inflammation and apoptosis of WI-38 cells induced by LPS, thus influencing the development of pneumonia. Our findings implied that NEAT1 might serve as a neoteric therapy target for pneumonia.
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Identifiers
31632562PMC6789249W2990144941What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.