Matriptase initiates activation of epidermal pro-kallikrein and disease onset in a mouse model of Netherton syndrome View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-08

AUTHORS

Katiuchia Uzzun Sales, Andrius Masedunskas, Alexandra L Bey, Amber L Rasmussen, Roberto Weigert, Karin List, Roman Szabo, Paul A Overbeek, Thomas H Bugge

ABSTRACT

Deficiency in the serine protease inhibitor LEKTI is the etiological origin of Netherton syndrome, which causes detachment of the stratum corneum and chronic inflammation. Here we show that the membrane protease matriptase initiates Netherton syndrome in a LEKTI-deficient mouse model by premature activation of a pro-kallikrein cascade. Auto-activation of pro-inflammatory pro-kallikrein-related peptidases that are associated with stratum corneum detachment was either low or undetectable, but they were efficiently activated by matriptase. Ablation of matriptase from LEKTI-deficient mice dampened inflammation, eliminated aberrant protease activity, prevented detachment of the stratum corneum, and improved the barrier function of the epidermis. These results uncover a pathogenic matriptase-pro-kallikrein pathway that could operate in several human skin and inflammatory diseases. More... »

PAGES

676

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng.629

    DOI

    http://dx.doi.org/10.1038/ng.629

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1028539439

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/20657595


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