ArticleEnvironmental health perspectives2011
Diesel particulate matter induces receptor for advanced glycation end-products (RAGE) expression in pulmonary epithelial cells, and RAGE signaling influences NF-κB-mediated inflammation.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Glycation and receptors: coming of AGE in the midst of danger.Nature reviews. Endocrinology · 2026Review
- Review
- Phagocytotic impairment of tissue-resident alveolar macrophages by diesel particulates drives pulmonary surfactant accumulation.Advanced biotechnology · 2026Article
- Carnosol exerts anti-inflammatory effects in pulpitis by inhibiting the RAGE/NF-κB signalling pathway.Scientific reports · 2025Article
- Differential Rates of Glycation Following Exposure to Unique Monosaccharides.International journal of molecular sciences · 2024Article
- The AGE-RAGE Axis and the Pathophysiology of Multimorbidity in COPD.Journal of clinical medicine · 2023Review
- Saponin attenuates diesel exhaust particle (DEP)-induced MUC5AC expression and pro-inflammatory cytokine upregulation via TLR4/TRIF/NF-κB signaling pathway in airway epithelium and ovalbumin (OVA)-sensitized mice.Journal of ginseng research · 2022Article
- A Study on Cough Sensitivity and Airway Inflammation in Patients with Sinobronchial Syndrome.Canadian respiratory journal · 2022Article
- Role of Innate Immune System in Environmental Lung Diseases.Current allergy and asthma reports · 2021Review
- Diesel Exhaust Particle Exposure Compromises Alveolar Macrophage Mitochondrial Bioenergetics.International journal of molecular sciences · 2019Article
- Transgenic up-regulation of Claudin-6 decreases fine diesel particulate matter (DPM)-induced pulmonary inflammation.Environmental science and pollution research international · 2018Article
- PM2.5 Induced the Expression of Fibrogenic Mediators via HMGB1-RAGE Signaling in Human Airway Epithelial Cells.Canadian respiratory journal · 2018Article
- Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets.Pharmacology & therapeutics · 2018Review
- Cytotoxicity of Air Pollutant 9,10-Phenanthrenequinone: Role of Reactive Oxygen Species and Redox Signaling.BioMed research international · 2018Review
- Intermittent Hypoxia Enhances THP-1 Monocyte Adhesion and Chemotaxis and Promotes M1 Macrophage Polarization via RAGE.BioMed research international · 2018Article
- Activation of Proinflammatory Responses in Cells of the Airway Mucosa by Particulate Matter: Oxidant- and Non-Oxidant-Mediated Triggering Mechanisms.Biomolecules · 2015Review
- RAGE/NF-κB signaling mediates lipopolysaccharide induced acute lung injury in neonate rat model.International journal of clinical and experimental medicine · 2015Article
- Conditionally induced RAGE expression by proximal airway epithelial cells in transgenic mice causes lung inflammation.Respiratory research · 2014Article
- RAGE/NF-κB pathway mediates lipopolysaccharide-induced inflammation in alveolar type I epithelial cells isolated from neonate rats.Inflammation · 2014Article
- Ambient particulate matter induces an exacerbation of airway inflammation in experimental asthma: role of interleukin-33.Clinical and experimental immunology · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundReceptors for advanced glycation end-products (RAGE) are cell-surface receptors expressed by alveolar type I (ATI) epithelial cells and are implicated in mechanisms of alveolar development and sustained pulmonary inflammation.
objectivesIn the present study, we tested the hypothesis that diesel particulate matter (DPM) up-regulates RAGE in rat ATI-like R3/1 cells and human primary small airway epithelial cells (SAECs), leading to an inflammatory response. METHODS AND
resultsUsing real-time reverse transcriptase polymerase chain reaction and immunoblotting, we found that RAGE mRNA and protein are up-regulated in cells exposed to DPM for 2 hr. Use of a luciferase reporter containing nuclear factor-κB (NF-κB) response elements revealed decreased NF-κB activation in cells transfected with small interfering RNA (siRNA) for RAGE (siRAGE) before DPM exposure compared with cells transfected with scrambled control siRNA (siControl). In addition, immunostaining revealed diminished nuclear translocation of NF-κB in DPM-exposed cells transfected with siRAGE compared with cells transfected with siControl before DPM stimulation. Enzyme-linked immunosorbent assay demonstrated that in R3/1 cells DPM induced secretion of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8), two cytokines induced by NF-κB and associated with leukocyte chemotaxis during an inflammatory response. Incorporating siRAGE was sufficient to significantly decrease DPM-induced MCP-1 and IL-8 secretion compared with cells transfected with siControl.
conclusionsThese data offer novel insights into potential mechanisms whereby RAGE influences pulmonary inflammation exacerbated by DPM exposure. Further research may demonstrate that molecules involved in RAGE signaling are potential targets in lessening the degree of particulate matter-induced exacerbations of inflammatory lung disease.
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