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    Loss of cortactin causes endothelial barrier dysfunction via disturbed adrenomedullin secretion and actomyosin contractility.

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    Authors
    García Ponce, Alexander
    Citalán Madrid, Alí F
    Vargas Robles, Hilda
    Chánez Paredes, Sandra
    Nava, Porfirio
    Betanzos, Abigail
    Zarbock, Alexander
    Rottner, Klemens cc
    Vestweber, Dietmar
    Schnoor, Michael
    Issue Date
    2016
    
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    Abstract
    Changes in vascular permeability occur during inflammation and the actin cytoskeleton plays a crucial role in regulating endothelial cell contacts and permeability. We demonstrated recently that the actin-binding protein cortactin regulates vascular permeability via Rap1. However, it is unknown if the actin cytoskeleton contributes to increased vascular permeability without cortactin. As we consistently observed more actin fibres in cortactin-depleted endothelial cells, we hypothesised that cortactin depletion results in increased stress fibre contractility and endothelial barrier destabilisation. Analysing the contractile machinery, we found increased ROCK1 protein levels in cortactin-depleted endothelium. Concomitantly, myosin light chain phosphorylation was increased while cofilin, mDia and ERM were unaffected. Secretion of the barrier-stabilising hormone adrenomedullin, which activates Rap1 and counteracts actomyosin contractility, was reduced in plasma from cortactin-deficient mice and in supernatants of cortactin-depleted endothelium. Importantly, adrenomedullin administration and ROCK1 inhibition reduced actomyosin contractility and rescued the effect on permeability provoked by cortactin deficiency in vitro and in vivo. Our data suggest a new role for cortactin in controlling actomyosin contractility with consequences for endothelial barrier integrity.
    Citation
    Loss of cortactin causes endothelial barrier dysfunction via disturbed adrenomedullin secretion and actomyosin contractility. 2016, 6:29003 Sci Rep
    Affiliation
    Department for Molecular Biomedicine, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
    Journal
    Scientific reports
    URI
    http://hdl.handle.net/10033/617265
    DOI
    10.1038/srep29003
    PubMed ID
    27357373
    Type
    Article
    Language
    en
    ISSN
    2045-2322
    ae974a485f413a2113503eed53cd6c53
    10.1038/srep29003
    Scopus Count
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    publications of the Research group: molecular cell biology (MZBI)

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