ArticlePloS one2011
Mucin secretion induced by titanium dioxide nanoparticles.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed.
- Silicon Carbide Nanowires Impair Mucociliary Clearance-Mediated Innate Immunity in Primary Human Bronchial Epithelial Cells.ACS nano · 2025Article
- The Stability and Anti-Angiogenic Properties of Titanium Dioxide Nanoparticles (TiOBiomolecules · 2022Article
- Review
- Particulate Matter Exposure Aggravates IL-17-Induced Eye and Nose Inflammation in an OVA/Poly(I:C) Mouse Model.Allergy, asthma & immunology research · 2022Article
- Metal nanomaterials: Immune effects and implications of physicochemical properties on sensitization, elicitation, and exacerbation of allergic disease.Journal of immunotoxicology · 2019Review
- Interactions of nanomaterials with ion channels and related mechanisms.British journal of pharmacology · 2019Review
- CeOThe Science of the total environment · 2018Article
- Probing Cellular Processes Using Engineered Nanoparticles.Bioconjugate chemistry · 2018Review
- Food-grade TiOJournal of nanobiotechnology · 2018Article
- The Toxicology of Engineered Nanomaterials in Asthma.Current environmental health reports · 2018Review
- Extracellular polymeric substances (EPS) producing and oil degrading bacteria isolated from the northern Gulf of Mexico.PloS one · 2018Article
- Effect of Engineered Nanoparticles on Exopolymeric Substances Release from Marine Phytoplankton.Nanoscale research letters · 2017Article
- Mechanistic insight into the impact of nanomaterials on asthma and allergic airway disease.Particle and fibre toxicology · 2017Review
- Engineered metal based nanoparticles and innate immunity.Clinical and molecular allergy : CMA · 2015Article
- Right or left: the role of nanoparticles in pulmonary diseases.International journal of molecular sciences · 2014Review
- Intracellular signal modulation by nanomaterials.Advances in experimental medicine and biology · 2014Review
- Cellular targets and mechanisms in the cytotoxic action of non-biodegradable engineered nanoparticles.Current drug metabolism · 2013Review
- Role of the Toll Like receptor (TLR) radical cycle in chronic inflammation: possible treatments targeting the TLR4 pathway.Molecular neurobiology · 2013Review
- Citrullination of proteins: a common post-translational modification pathway induced by different nanoparticles in vitro and in vivo.Nanomedicine (London, England) · 2012Article
- Models for oral uptake of nanoparticles in consumer products.Toxicology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Nanoparticle (NP) exposure has been closely associated with the exacerbation and pathophysiology of many respiratory diseases such as Chronic Obstructive Pulmonary Disease (COPD) and asthma. Mucus hypersecretion and accumulation in the airway are major clinical manifestations commonly found in these diseases. Among a broad spectrum of NPs, titanium dioxide (TiO(2)), one of the PM10 components, is widely utilized in the nanoindustry for manufacturing and processing of various commercial products. Although TiO(2) NPs have been shown to induce cellular nanotoxicity and emphysema-like symptoms, whether TiO(2) NPs can directly induce mucus secretion from airway cells is currently unknown. Herein, we showed that TiO(2) NPs (<75 nm) can directly stimulate mucin secretion from human bronchial ChaGo-K1 epithelial cells via a Ca(2+) signaling mediated pathway. The amount of mucin secreted was quantified with enzyme-linked lectin assay (ELLA). The corresponding changes in cytosolic Ca(2+) concentration were monitored with Rhod-2, a fluorescent Ca(2+) dye. We found that TiO(2) NP-evoked mucin secretion was a function of increasing intracellular Ca(2+) concentration resulting from an extracellular Ca(2+) influx via membrane Ca(2+) channels and cytosolic ER Ca(2+) release. The calcium-induced calcium release (CICR) mechanism played a major role in further amplifying the intracellular Ca(2+) signal and in sustaining a cytosolic Ca(2+) increase. This study provides a potential mechanistic link between airborne NPs and the pathoetiology of pulmonary diseases involving mucus hypersecretion.
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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 Socratic graph.