ArticleParticle and fibre toxicology2017
Silica nanoparticles inhibit the cation channel TRPV4 in airway epithelial cells.
Article in Particle and fibre toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Potential role of theFrontiers in genetics · 2026Article
- Epithelium-derived exosomes promote silica nanoparticles-induced pulmonary fibroblast activation and collagen deposition via modulating fibrotic signaling pathways and their epigenetic regulations.Journal of nanobiotechnology · 2024Article
- Review
- Pulmonary Toxicity of Silica Linked to Its Micro- or Nanometric Particle Size and Crystal Structure: A Review.Nanomaterials (Basel, Switzerland) · 2022Review
- NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction.Antioxidants (Basel, Switzerland) · 2022Article
- Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Nano-silica particles synergistically IgE-mediated mast cell activation exacerbating allergic inflammation in mice.Frontiers in immunology · 2022Article
- Silica Nanoparticles Inhibit Responses to ATP in Human Airway Epithelial 16HBE Cells.International journal of molecular sciences · 2021Article
- CaCells · 2021Review
- TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021Review
- Biological effects of inhaled hydraulic fracturing sand dust. IV. Pulmonary effects.Toxicology and applied pharmacology · 2020Article
- Crystalline silica particles cause rapid NLRP3-dependent mitochondrial depolarization and DNA damage in airway epithelial cells.Particle and fibre toxicology · 2020Article
- Ultrafine silicon dioxide nanoparticles cause lung epithelial cells apoptosis via oxidative stress-activated PI3K/Akt-mediated mitochondria- and endoplasmic reticulum stress-dependent signaling pathways.Scientific reports · 2020Article
- TRPV4: A Physio and Pathophysiologically Significant Ion Channel.International journal of molecular sciences · 2020Review
- Mechanisms of ultrafine particle-induced respiratory health effects.Experimental & molecular medicine · 2020Review
- Interactions of nanomaterials with ion channels and related mechanisms.British journal of pharmacology · 2019Review
- Transient Receptor Potential Ion Channel-Dependent Toxicity of Silica Nanoparticles and Poly(amido amine) Dendrimers.The Journal of pharmacology and experimental therapeutics · 2019Article
- The puzzling issue of silica toxicity: are silanols bridging the gaps between surface states and pathogenicity?Particle and fibre toxicology · 2019Article
- Calcium-dependent cyto- and genotoxicity of nickel metal and nickel oxide nanoparticles in human lung cells.Particle and fibre toxicology · 2018Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSilica nanoparticles (SiNPs) have numerous beneficial properties and are extensively used in cosmetics and food industries as anti-caking, densifying and hydrophobic agents. However, the increasing exposure levels experienced by the general population and the ability of SiNPs to penetrate cells and tissues have raised concerns about possible toxic effects of this material. Although SiNPs are known to affect the function of the airway epithelium, the molecular targets of these particles remain largely unknown. Given that SiNPs interact with the plasma membrane of epithelial cells we hypothesized that they may affect the function of Transient Receptor Potential Vanilloid 4 (TRPV4), a cation-permeable channel that regulates epithelial barrier function. The main aims of this study were to evaluate the effects of SiNPs on the activation of TRPV4 and to determine whether these alter the positive modulatory action of this channel on the ciliary beat frequency in airway epithelial cells.
resultsUsing fluorometric measurements of intracellular Ca
conclusionsOur results show that SiNPs inhibit TRPV4 activation, and that this effect may impair the positive modulatory action of the stimulation of this channel on the ciliary function in airway epithelial cells. These findings unveil the cation channel TRPV4 as a primary molecular target of SiNPs.
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