ArticleParticle and fibre toxicology2024
Epithelial MAPK signaling directs endothelial NRF2 signaling and IL-8 secretion in a tri-culture model of the alveolar-microvascular interface following diesel exhaust particulate (DEP) exposure.
Article in Particle and fibre toxicology, 2024. 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, 12 citations in OpenAlex.
- In vitro approaches to assess respiratory toxicity from volatile organic compounds: an in-depth review.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Breathing lung-on-chip: a versatile tool for assessing respiratory toxicity across multiple therapeutic modalities.Archives of toxicology · 2026Article
- Seawater drowning induced acute lung injury: new insights from novel mouse models and micro-CT imaging.Open medicine (Warsaw, Poland) · 2026Article
- DifferentialACS ES&T air · 2025Article
- Immune-Epigenetic Effects of Environmental Pollutants: Mechanisms, Biomarkers, and Transgenerational Impact.Current issues in molecular biology · 2025Review
- Wildfire-relevant woodsmoke and extracellular vesicles (EVs): Alterations in EV proteomic signatures involved in extracellular matrix degradation and tissue injury in airway organotypic models.Environmental research · 2025Article
- Targeting the AMPK/Nrf2 Pathway: A Novel Therapeutic Approach for Acute Lung Injury.Journal of inflammation research · 2024Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundParticulate matter 2.5 (PM
methodsAn in vitro, tri-culture model of the ACR, incorporating alveolar-like epithelial cells (NCI-H441), pulmonary fibroblasts (IMR90), and pulmonary microvascular endothelial cells (HULEC) was developed to investigate cell type-specific molecular responses to a PM
resultsAlveolar epithelial barrier formation was not perturbed by the 24 h DEP exposure. Despite no alteration in barrier formation, we demonstrate that alveolar epithelial DEP exposure induces transcriptional and protein changes in both the alveolar epithelial cells and the underlying microvascular endothelial cells. Specifically, we show that the underlying microvascular endothelial cells develop redox dysfunction and increase proinflammatory cytokine secretion. Furthermore, we demonstrate that alveolar epithelial MAPK signaling modulates the activation of NRF2 and IL-8 secretion in the underlying microvascular endothelial cells.
conclusionsEndothelial redox dysfunction and increased proinflammatory cytokine secretion are two common events in respiratory disease development. These findings highlight new, cell-type specific roles of the alveolar epithelium and microvascular endothelium in the ACR in respiratory disease development following PM
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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.