Ambient particulate matter affects occludin distribution and increases alveolar transepithelial electrical conductance
Identifieur interne : 001583 ( Main/Exploration ); précédent : 001582; suivant : 001584Ambient particulate matter affects occludin distribution and increases alveolar transepithelial electrical conductance
Auteurs : Juan C. Caraballo ; Cecilia Yshii ; Whitney Westphal ; Thomas Moninger [États-Unis] ; Alejandro P. Comellas [États-Unis]Source :
- Respirology [ 1323-7799 ] ; 2011-02.
English descriptors
- Teeft :
- Adenovirus, Alveolar, Alveolar barrier, Alveolar epithelial barrier, Alveolar epithelial cells, Alveolar epithelial dysfunction, Antioxidant, Antioxidant enzymes, Asian society, Authors respirology, Biol, Catalase, Cell death, Diesel exhaust particles, Dysfunction, Empty adenovirus, Endosomal, Endosomal compartments, Epithelial, Epithelial cells, Free radic, Independent experiments, Individual experiments, Lanthanum nitrate, Lung function, Mitochondrial, Mnsod, Occludin, Occludin abundance, Occludin reduction, Overexpression, Particulate, Particulate matter, Permeability, Plasma membrane, Plasmid, Pulmonary function, Quantitative analysis, Reactive oxygen species, Representative blots, Respirology, Respirology respirology, Results show, Streptavidin beads, Surface proteins, Tight junctions, Tio2, Total cell lysate, Toxicol, Transmission electron microscopy, Western blot.
Abstract
Background and objective: Inhaled particulate matter (PM) causes lung inflammation and epithelial dysfunction. However, the direct effect of PM on alveolar epithelial barrier integrity is not well understood. Our aim is to determine whether PM exposure affects the alveolar epithelial cells (AEC) transepithelial electrical conductance (Gt) and tight junction (TJ) proteins. Methods: Human AEC (A549) and primary rat AEC were exposed to PM of <10 µm in size (PM10) and diesel exhaust particles (DEP), using titanium dioxide (TiO2) as a control for particle size effects. Gt and permeability to fluorescein isothiocyanate‐dextran (FITC‐Dextran) were measured to assess barrier integrity. TJ integrity was evaluated by analysing penetration of Lanthanum nitrate (La3+) under transmission electron microscopy. Surface proteins were labelled with biotin and analysed by western blot. Immunofluorescence was performed to assess colocalization of TJ proteins including occludin and zonula occludens‐1 (ZO‐1). PM induced dissociation of occludin‐ZO‐1 was evaluated by co‐immunoprecipitation. Results: PM10 and DEP increased Gt and disrupted TJ after 3 h of treatment. PM10 and DEP induced occludin internalization from the plasma membrane into endosomal compartments and dissociation of occludin from ZO‐1. Overexpression of antioxidant enzymes manganese superoxide dismutase (MnSOD) and catalase, prevented PM‐induced Gt increase, occludin reduction from the plasma membrane and its dissociation from ZO‐1. Conclusions: PM induces alveolar epithelial dysfunction in part via occludin reduction at the plasma membrane and ZO‐1 dissociation in AEC. Furthermore, these effects are prevented by overexpression of two different antioxidant enzymes.
This work studies the effects of particulate matter and diesel exhaust particles on alveolar barrier integrity in vitro. Our results show that these particles alter tight junction integrity, specifically the occludin and ZO‐1 association. These effects are prevented by blocking of mitochondrial ROS production, suggesting a central role of this organelle in the effects observed.
Url:
DOI: 10.1111/j.1440-1843.2010.01910.x
Affiliations:
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However, the direct effect of PM on alveolar epithelial barrier integrity is not well understood. Our aim is to determine whether PM exposure affects the alveolar epithelial cells (AEC) transepithelial electrical conductance (Gt) and tight junction (TJ) proteins. Methods: Human AEC (A549) and primary rat AEC were exposed to PM of <10 µm in size (PM10) and diesel exhaust particles (DEP), using titanium dioxide (TiO2) as a control for particle size effects. Gt and permeability to fluorescein isothiocyanate‐dextran (FITC‐Dextran) were measured to assess barrier integrity. TJ integrity was evaluated by analysing penetration of Lanthanum nitrate (La3+) under transmission electron microscopy. Surface proteins were labelled with biotin and analysed by western blot. Immunofluorescence was performed to assess colocalization of TJ proteins including occludin and zonula occludens‐1 (ZO‐1). PM induced dissociation of occludin‐ZO‐1 was evaluated by co‐immunoprecipitation. Results: PM10 and DEP increased Gt and disrupted TJ after 3 h of treatment. PM10 and DEP induced occludin internalization from the plasma membrane into endosomal compartments and dissociation of occludin from ZO‐1. Overexpression of antioxidant enzymes manganese superoxide dismutase (MnSOD) and catalase, prevented PM‐induced Gt increase, occludin reduction from the plasma membrane and its dissociation from ZO‐1. Conclusions: PM induces alveolar epithelial dysfunction in part via occludin reduction at the plasma membrane and ZO‐1 dissociation in AEC. Furthermore, these effects are prevented by overexpression of two different antioxidant enzymes.</div><div type="abstract">This work studies the effects of particulate matter and diesel exhaust particles on alveolar barrier integrity in vitro. Our results show that these particles alter tight junction integrity, specifically the occludin and ZO‐1 association. These effects are prevented by blocking of mitochondrial ROS production, suggesting a central role of this organelle in the effects observed.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Iowa</li></region><settlement><li>Iowa City</li></settlement><orgName><li>Université de l'Iowa</li></orgName></list><tree><noCountry><name sortKey="Caraballo, Juan C" sort="Caraballo, Juan C" uniqKey="Caraballo J" first="Juan C." last="Caraballo">Juan C. Caraballo</name><name sortKey="Westphal, Whitney" sort="Westphal, Whitney" uniqKey="Westphal W" first="Whitney" last="Westphal">Whitney Westphal</name><name sortKey="Yshii, Cecilia" sort="Yshii, Cecilia" uniqKey="Yshii C" first="Cecilia" last="Yshii">Cecilia Yshii</name></noCountry><country name="États-Unis"><region name="Iowa"><name sortKey="Moninger, Thomas" sort="Moninger, Thomas" uniqKey="Moninger T" first="Thomas" last="Moninger">Thomas Moninger</name></region><name sortKey="Comellas, Alejandro P" sort="Comellas, Alejandro P" uniqKey="Comellas A" first="Alejandro P." last="Comellas">Alejandro P. Comellas</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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