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    Loss of epidermal AP1 transcription factor function reduces filaggrin level, alters chemokine expression and produces an ichthyosis-related phenotype

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    Author
    Young, C.A.
    Rorke, E.A.
    Adhikary, G.
    Date
    2017
    Journal
    Cell death & disease
    Type
    Article
    
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    See at
    https://doi.org/10.1038/cddis.2017.238
    Abstract
    AP1 transcription factors are important controllers of epidermal differentiation. Multiple family members are expressed in the epidermis in a differentiation-dependent manner, where they function to regulate gene expression. To study the role of AP1 factor signaling, TAM67 (dominant-negative c-jun) was inducibly expressed in the suprabasal epidermis. The TAM67-positive epidermis displays keratinocyte hyperproliferation, hyperkeratosis and parakeratosis, delayed differentiation, extensive subdermal vasodilation, nuclear loricrin localization, tail and digit pseudoainhum and reduced filaggrin level. These changes are associated with increased levels of IFN?, CCL3, CCL5, CXCL9, CXCL10, and CXCL11 (Th1-associated chemokines), and CCL1, CCL2, CCL5 and CCL11 (Th2-associated chemokines) in the epidermis and serum. S100A8 and S100A9 protein levels are also markedly elevated. These changes in epidermal chemokine level are associated with increased levels of the corresponding chemokine mRNA. The largest increases were observed for CXCL9, CXCL10, CXCL11, and S100A8 and S100A9. To assess the role of CXCL9, CXCL10, CXCL11, which bind to CXCR3, on phenotype development, we expressed TAM67 in CXCR3 knockout mice. Using a similar strategy, we examine the role of S100A8 and S100A9. Surprisingly, loss of CXCR3 or S100A8/A9 did not attenuate phenotype development. These studies suggest that interfering with epidermal AP1 factor signaling initiates a loss of barrier function leading to enhanced epidermal chemokine production, but that CXCR3 and S100A8/A9 do not mediate the phenotypic response.
    Keyword
    Ichthyosis--genetics
    Intermediate Filament Proteins--genetics
    Peptide Fragments--genetics
    Proto-Oncogene Proteins c-jun--genetics
    Th1-Th2 Balance--genetics
    Transcription Factor AP-1--genetics
    Epidermis
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85043361409&doi=10.1038%2fcddis.2017.238&partnerID=40&md5=2a2c1174c7f53456d679c46bb0034950; http://hdl.handle.net/10713/11349
    ae974a485f413a2113503eed53cd6c53
    10.1038/cddis.2017.238
    Scopus Count
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    UMB Open Access Articles 2017

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