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Related Experiment Video

Updated: Nov 1, 2025

Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures
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circ_0038467 promotes PM2.5-induced bronchial epithelial cell dysfunction.

Xuan Jin1,2, Li Wang1, Mingzhu Yang3

  • 1Department of Pediatrics, Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, No. 2, Weiyang West Road, Xianyang 712000, Shaan'xi, China.

Open Medicine (Warsaw, Poland)
|June 24, 2021
PubMed
Summary

Particulate matter (PM2.5) exposure increases circ_0038467 and decreases miR-138-1-3p, leading to lung cell damage. Targeting circ_0038467 may offer a therapeutic strategy for air pollution-induced lung dysfunction.

Keywords:
BEAS-2BNF-κB pathwaycirc_0038467lung dysfunctionmiR-138-1-3p

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Area of Science:

  • Environmental toxicology
  • Molecular biology
  • Cellular mechanisms of lung injury

Background:

  • Particulate matter (PM2.5) is a major air pollutant linked to respiratory diseases.
  • Understanding the molecular mechanisms of PM2.5-induced lung dysfunction is crucial for developing effective interventions.

Purpose of the Study:

  • To elucidate the toxicological mechanisms of PM2.5-induced lung dysfunction.
  • To investigate the roles of circ_0038467 and miR-138-1-3p in PM2.5-induced lung epithelial cell injury.

Main Methods:

  • Real-time quantitative PCR (RT-qPCR) to measure circ_0038467 and miR-138-1-3p expression in PM2.5-exposed BEAS-2B cells.
  • Cell counting kit-8, flow cytometry, western blot, and ELISA to assess cell proliferation, apoptosis, and inflammatory cytokine release (IL-6, IL-8).
  • Dual-luciferase reporter assay, RNA immunoprecipitation, and pull-down assays to confirm the interaction between circ_0038467 and miR-138-1-3p.

Main Results:

  • PM2.5 exposure upregulated circ_0038467 and downregulated miR-138-1-3p in BEAS-2B cells in a time- and dose-dependent manner.
  • Knockdown of circ_0038467 reversed PM2.5-induced cell death and inflammation, while restoration of miR-138-1-3p attenuated PM2.5-induced cell injury.
  • circ_0038467 directly targets miR-138-1-3p, and inhibition of miR-138-1-3p partially reversed the protective effects of circ_0038467 knockdown.

Conclusions:

  • circ_0038467 acts as a molecular sponge for miR-138-1-3p, contributing to PM2.5-induced lung epithelial cell damage.
  • The circ_0038467/miR-138-1-3p axis plays a critical role in the pathogenesis of air pollution-induced lung dysfunction.
  • circ_0038467 represents a potential therapeutic target for mitigating lung injury caused by air pollution.