ArticleThe Kaohsiung journal of medical sciences2020
Analysis the effect of miR-141-3p/HMGB1 in LPS-induced mucus production and the apoptosis in nasal epithelial cells.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- H1FX as a novel biomarker linking pan-apoptosis to immune dysregulation in allergic rhinitis.European journal of medical research · 2026Article
- HMGB1 as a Key Modulator in Nasal Inflammatory Disorders: A Narrative Review.Journal of clinical medicine · 2025Review
- miR-141-3p-loaded extracellular vesicles ameliorate intrahepatic bile duct stone disease by decreasing MUC5AC expressionIntractable & rare diseases research · 2025Article
- miR-6089 Alleviates Inflammation and Cell Apoptosis Through Modulating the TLR4 Pathway in Mite-Sensitized Allergic Rhinitis.Journal of inflammation research · 2025Article
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- Review
- Analysis the effect of miR-141-3p/HMGB1 in LPS-induced mucus production and the apoptosis in nasal epithelial cells.The Kaohsiung journal of medical sciences · 2020Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic rhinitis (AR) is an allergic disease characterized by immunoglobulin E (IgE)-mediated type I hypersensitivity disorder. In the current study, we illuminated the potential roles of microRNA-141-3p (miR-141-3p) in lipopolysaccharide (LPS)-induced mucus production and the apoptosis in nasal epithelial cells (NECs). We demonstrated that miR-141-3p was significantly downregulated in nasal tissues from patients with AR and LPS-treated NECs. Upregulation of miR-141-3p decreased the level of mucin 5AC (MUC5AC) in LPS-treated NECs and induced NECs apoptosis. High Mobility Group Box 1 (HMGB1) was proved as a target of miR-141-3p and miR-141-3p negatively regulated its expression. In addition, we observed that HMGB1 was overexpressed in nasal mucosal tissues from patients with AR and LPS-treated NECs. Finally, we proved that miR-141-3p decreased the level of MUAC5AC in LPS-treated NECs through regulating HMGB1. In conclusion, miR-141-3p inhibited LPS-induced MUAC5AC production and the apoptosis of LPS-treated NECs by targeting HMGB1.
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Registered trials
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