ArticleMolecular biology of the cell2015
Silica particles cause NADPH oxidase-independent ROS generation and transient phagolysosomal leakage.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Silica Promotes Silicosis via the ROS/NF-κB p65 Signaling-Activated Hypoxia-Lactate Axis in Rats.Journal of applied toxicology : JAT · 2026Article
- Glycoprotein-induced phase separation drives unconventional secretion of galectin-3.Nature communications · 2026Article
- Regulation of NLRP3 inflammasome signaling in Alzheimer's disease: emerging neuroprotective role of phytochemicals.Inflammopharmacology · 2026Review
- Particle dissolution rate controls macrophage response and drug release from mesoporous silica inhalation carriers.Scientific reports · 2026Article
- The spectrum of lysosomal stress and damage responses: from mechanosensing to inflammation.EMBO reports · 2025Review
- Unveiling the threat of crystalline silica on the cardiovascular system. A comprehensive review of the current knowledge.Frontiers in cardiovascular medicine · 2025Review
- CaProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Macrophage-derived exosomal HMGB3 regulates silica-induced pulmonary inflammation by promoting M1 macrophage polarization and recruitment.Particle and fibre toxicology · 2024Article
- High-fat Western diet alters crystalline silica-induced airway epithelium ion transport but not airway smooth muscle reactivity.BMC research notes · 2024Article
- Article
- Yangqing Chenfei formula alleviates silica-induced pulmonary inflammation in rats by inhibiting macrophage M1 polarization.Chinese medicine · 2023Article
- Cellular uptake and retention studies of silica nanoparticles utilizing senescent fibroblasts.Scientific reports · 2023Article
- Crystalline silica-induced proinflammatory eicosanoid storm in novel alveolar macrophage model quelled by docosahexaenoic acid supplementation.Frontiers in immunology · 2023Article
- Engineered Mesoporous Silica-Based Core-Shell Nanoarchitectures for Synergistic Chemo-Photodynamic Therapies.International journal of molecular sciences · 2022Article
- Pulmonary Toxicity of Silica Linked to Its Micro- or Nanometric Particle Size and Crystal Structure: A Review.Nanomaterials (Basel, Switzerland) · 2022Review
- High-fat Western diet consumption exacerbates silica-induced pulmonary inflammation and fibrosis.Toxicology reports · 2022Article
- Think Beyond Particle Cytotoxicity: When Self-Cellular Components Released After Immunogenic Cell Death Explain Chronic Disease Development.Frontiers in toxicology · 2022Review
- Genome-wide mRNA profiling identifies the NRF2-regulated lymphocyte oxidative stress status in patients with silicosis.Journal of occupational medicine and toxicology (London, England) · 2021Article
- Cannabidiol modulation of oxidative stress and signalling.Neuronal signaling · 2021Review
- Randall's plaque and calcium oxalate stone formation: role for immunity and inflammation.Nature reviews. Nephrology · 2021Review
Corrections and comments
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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
Chronic inhalation of silica particles causes lung fibrosis and silicosis. Silica taken up by alveolar macrophages causes phagolysosomal membrane damage and leakage of lysosomal material into the cytoplasm to initiate apoptosis. We investigated the role of reactive oxygen species (ROS) in this membrane damage by studying the spatiotemporal generation of ROS. In macrophages, ROS generated by NADPH oxidase 2 (NOX2) was detected in phagolysosomes containing either silica particles or nontoxic latex particles. ROS was only detected in the cytoplasm of cells treated with silica and appeared in parallel with an increase in phagosomal ROS, as well as several hours later associated with mitochondrial production of ROS late in apoptosis. Pharmacological inhibition of NOX activity did not prevent silica-induced phagolysosomal leakage but delayed it. In Cos7 cells, which do not express NOX2, ROS was detected in silica-containing phagolysosomes that leaked. ROS was not detected in phagolysosomes containing latex particles. Leakage of silica-containing phagolysosomes in both cell types was transient, and after resealing of the membrane, endolysosomal fusion continued. These results demonstrate that silica particles can generate phagosomal ROS independent of NOX activity, and we propose that this silica-generated ROS can cause phagolysosomal leakage to initiate apoptosis.
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