Fachbereich Veterinärmedizin


Service-Navigation

    Publikationsdatenbank

    CLCA2 is Overexpressed in Psoriatic but not in Atopic Dermatitis Mouse Skin Models (2017)

    Art
    Poster
    Autoren
    Fürstenau, J (WE 12)
    Pischon, H (WE 12)
    Dietert, K (WE 12)
    Radbruch, M (WE 12)
    Gruber, A.D. (WE 12)
    Mundhenk, Lars (WE 12)
    Kongress
    Joint European Congress of the ECVP and ESVP
    Bologna, 07. – 10.09.2016
    Quelle
    Journal of Comparative Pathology; 156(1) — S. 137
    ISSN: 0021-9975
    Sprache
    Englisch
    Verweise
    DOI: 10.1016/j.jcpa.2016.11.251
    Kontakt
    Institut für Tierpathologie

    Robert-von-Ostertag-Str. 15
    Gebäude 12
    14163 Berlin
    Tel.+49 30 838 62450 Fax.+49 30 838 62522

    Abstract / Zusammenfassung

    Introduction: CLCA2 is expressed in keratinocytes and is thought to be required for epidermal differentiation. Terminal epidermal differentiation proteins like filaggrin have a pivotal role in skin barrier function and are highly regulated in skin diseases. Here, we studied the expression pattern of CLCA2 in murine models of atopic dermatitis and psoriasis.

    Materials and Methods: Atopic dermatitis or psoriasis-like diseases were induced in hairless SKH-1 mice via oxazolone sensitization or in BALB/c mice via topical application of imiquimod, respectively. The expression pattern of CLCA2 was characterized via RT-qPCR and immunohistochemistry in the inflamed murine skin and healthy controls.

    Results: Expression of CLCA2 mRNA was approximately five-times higher in psoriasis-like skin compared with the skin of healthy controls, while it was unchanged in the atopic dermatitis model. This disease-specific regulation was confirmed at the protein level in both models.

    Conclusions: CLCA2 is overexpressed only in the psoriatic skin model, but not in atopic dermatitis. This difference is consistent with hyperkeratosis-associated increased expression of other terminal differential proteins in psoriasis in contrast to atopic dermatitis. Our results support the notion that CLCA2 is a terminal differentiation protein.