ArticleInternational journal of nanomedicine2011
Translocation of PEGylated quantum dots across rat alveolar epithelial cell monolayers.
Article in International journal of nanomedicine, 2011. 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, 17 citations in OpenAlex.
- Asymmetric distribution of dynamin-2 and β-catenin relative to tight junction spikes in alveolar epithelial cells.Tissue barriers · 2021Article
- Alveolar epithelial cell processing of nanoparticles activates autophagy and lysosomal exocytosis.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Progress and future of in vitro models to study translocation of nanoparticles.Archives of toxicology · 2015Review
- Translocation of gold nanoparticles across the lung epithelial tissue barrier: Combining in vitro and in silico methods to substitute in vivo experiments.Particle and fibre toxicology · 2015Article
- Claudin 4 knockout mice: normal physiological phenotype with increased susceptibility to lung injury.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Effect of modifying quantum dot surface charge on airway epithelial cell uptake in vitro.Nanotoxicology · 2013Article
- Nanoparticle translocation across mouse alveolar epithelial cell monolayers: species-specific mechanisms.Nanomedicine : nanotechnology, biology, and medicine · 2013Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIn this study, primary rat alveolar epithelial cell monolayers (RAECM) were used to investigate transalveolar epithelial quantum dot trafficking rates and underlying transport mechanisms.
methodsTrafficking rates of quantum dots (PEGylated CdSe/ZnS, core size 5.3 nm, hydrodynamic size 25 nm) in the apical-to-basolateral direction across RAECM were determined. Changes in bioelectric properties (ie, transmonolayer resistance and equivalent active ion transport rate) of RAECM in the presence or absence of quantum dots were measured. Involvement of endocytic pathways in quantum dot trafficking across RAECM was assessed using specific inhibitors (eg, methyl-β-cyclodextrin, chlorpromazine, and dynasore for caveolin-, clathrin-, and dynamin-mediated endocytosis, respectively). The effects of lowering tight junctional resistance on quantum dot trafficking were determined by depleting Ca(2+) in apical and basolateral bathing fluids of RAECM using 2 mM EGTA. Effects of temperature on quantum dot trafficking were studied by lowering temperature from 37°C to 4°C.
resultsApical exposure of RAECM to quantum dots did not elicit changes in transmonolayer resistance or ion transport rate for up to 24 hours; quantum dot trafficking rates were not surface charge-dependent; methyl-β-cyclodextrin, chlorpromazine, and dynasore did not decrease quantum dot trafficking rates; lowering of temperature decreased transmonolayer resistance by approximately 90% with a concomitant increase in quantum dot trafficking by about 80%; and 24 hours of treatment of RAECM with EGTA decreased transmonolayer resistance by about 95%, with increased quantum dot trafficking of up to approximately 130%.
conclusionThese data indicate that quantum dots do not injure RAECM and that quantum dot trafficking does not appear to take place via endocytic pathways involving caveolin, clathrin, or dynamin. We conclude that quantum dot translocation across RAECM takes place via both transcellular and paracellular pathways and, based on comparison with our prior studies, interactions of nanoparticles with RAECM are strongly dependent on nanoparticle composition and surface properties.
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