ArticleGenes & genomics2021
Long non-coding RNA NEAT1 promotes lipopolysaccharide-induced acute lung injury by regulating miR-424-5p/MAPK14 axis.
Article in Genes & genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Decoding the lncRNA-miRNA-mRNA network in sepsis-induced lung injury: from pathogenesis to extracellular vesicle-based therapy.Frontiers in immunology · 2026Review
- Dauriporphine inhibited lung cancer cell viability, motility, and energy metabolism through the miR-424-5p/MAPK14 axis.Hereditas · 2025Article
- LncRNA NEAT1 protects uremic toxin-induced intestinal epithelial barrier injury by regulating miR-122-5p/Occludin axis.PloS one · 2025Article
- Article
- Circular RNA KIAA0564 Serves as a Competitive Endogenous RNA for MicroRNA-424-5p, Mediating the Expression of Lysine Demethylase 4a, Thereby Facilitating Intervertebral Disc Degeneration.Applied biochemistry and biotechnology · 2024Article
- METTL3 aggravates cell damage induced by Streptococcus pneumoniae via the NEAT1/CTCF/MUC19 axis.The Kaohsiung journal of medical sciences · 2024Article
- Breviscapine Reduces Sepsis-Induced Acute Lung Injury by Targeting CASP8 to Regulate Neutrophil Apoptosis and Inflammation.Journal of inflammation research · 2024Article
- Functional roles of circular RNAs in lung injury.Frontiers in pharmacology · 2024Review
- MiR-424/TGIF2-Mediated Pro-Fibrogenic Responses in Oral Submucous Fibrosis.International journal of molecular sciences · 2023Article
- MicroRNA-424-5p Alleviates Isoflurane Anesthesia-Induced Neurotoxicity in Human Embryonic Stem Cell-Derived Neurons by Targeting FASN.Computational and mathematical methods in medicine · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMany long non-coding RNAs (lncRNAs) have been suggested to play critical roles in acute lung injury (ALI) pathogenesis, including lncRNA nuclear enriched abundant transcript 1 (NEAT1).
objectiveWe aimed to further elucidate the functions and molecular mechanism of NEAT1 in ALI.
methodsHuman pulmonary alveolar epithelial cells (HPAEpiCs) stimulated by lipopolysaccharide (LPS) were served as a cellular model of ALI. Cell viability and cell apoptosis were determined by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The expression of NEAT1, microRNA-424-5p (miR-424-5p), and mitogen-activated protein kinase 14 (MAPK14) was measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot analysis. Caspase activity was determined by caspase activity kit. The inflammatory responses were evaluated using enzyme-linked immunosorbent assay (ELISA). The oxidative stress factors were analyzed by corresponding kits.
resultsNEAT1 was upregulated in LPS-stimulated HPAEpiCs. NEAT1 knockdown weakened LPS-induced injury by inhibiting apoptosis, inflammation and oxidative stress in HPAEpiCs. Moreover, miR-424-5p was a direct target of NEAT1, and its knockdown reversed the effects caused by NEAT1 knockdown in LPS-induced HPAEpiCs. Furthermore, MAPK14 was a downstream target of miR-424-5p, and its overexpression attenuated the effects of miR-424-5p on reduction of LPS-induced injury in HPAEpiCs. Besides, NEAT1 acted as a sponge of miR-424-5p to regulate MAPK14 expression.
conclusionNEAT1 knockdown alleviated LPS-induced injury of HPAEpiCs by regulating miR-424-5p/MAPK14 axis, which provided a potential therapeutic target for the treatment of ALI.
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