ArticleOpen medicine (Warsaw, Poland)2021
circ_0038467 promotes PM2.5-induced bronchial epithelial cell dysfunction.
Article in Open medicine (Warsaw, Poland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Development of a three-dimensional airway organoid-pillar dish (3D AO-PD) platform for particulate matter-induced airway toxicity analysis.Materials today. Bio · 2025Article
- MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy.Frontiers in pharmacology · 2022Article
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Authors and funding
3 authors.
Funding
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Abstract
purposeThis study was to explore the toxicological mechanisms by which PM2.5 causes lung dysfunction.
methodsThe expression of circ_0038467 and miR-138-1-3p in PM2.5-induced human bronchial epithelial cell line BEAS-2B was detected by RT-qPCR. The effects of circ_0038467 and miR-138-1-3p on proliferation, apoptosis, and inflammatory cytokines (IL-6 and IL-8) in PM2.5-induced BEAS-2B were determined using cell counting kit-8, flow cytometry, western blot, and enzyme-linked immunosorbent assay, respectively. The levels of nuclear factor kappa B (NF-κB) pathway-related protein were also analyzed by western blot. The binding interaction between circ_0038467 and miR-138-1-3p was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay and pull-down assay.
resultscirc_0038467 expression was increased by PM2.5 treatment in BEAS-2B cells in time- and dose-dependent methods, and knockdown of circ_0038467 reversed PM2.5-triggered BEAS-2B cell death and inflammatory response. miR-138-1-3p was decreased by PM2.5 treatment, and restoration of miR-138-1-3p attenuated PM2.5-induced BEAS-2B cell injury. In a mechanical study, we found circ_0038467 directly bound to miR-138-1-3p, and further rescue experiments exhibited miR-138-1-3p inhibition partially overturned the regulatory functions of circ_0038467 knockdown in PM2.5-induced BEAS-2B cells.
conclusioncirc_0038467 provided a potential therapeutic strategy for future clinic intervention in air pollution-triggered lung dysfunction.
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