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Caspase-14-deficient mice are more prone to the development of parakeratosis

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Abstract
Caspase-14 is an important protease in the proper formation of a fully functional skin barrier. Newborn mice that are deficient in caspase-14 exhibit increased transepidermal water loss and are highly sensitive to UVB-induced photodamage. Decreased caspase-14 expression and incomplete caspase-14 processing in lesional psoriatic parakeratotic stratum corneum has been reported previously. In this study, we show that caspase-14-deficient skin frequently displays incompletely cornified cells in the transitional zone between the granular and the cornified layers, pointing to a delay in cornification. We also demonstrate that after challenge of epidermal permeability barrier function by repetitive acetone treatment, a higher incidence of large parakeratotic plaques was observed in caspase-14-deficient skin. Furthermore, caspase-14-deficient mice are more prone than control mice to the development of parakeratosis upon induction of psoriasis-like dermatitis by imiquimod treatment. These results glow that lack of caspase-14 expression predisposes to the development of parakeratosis and that caspase-14 ha an important role in keratinocyte; terminal differentiation and the maintenance of normal stratum corneum, especially in conditions causing epidermal hyperproliferation.
Keywords
KERATINOCYTES, EXPRESSION, INFLAMMATION, IMIQUIMOD, DEGRADATION, PSORIASIS, SKIN, WATER-LOSS, HUMAN EPIDERMIS, BARRIER FUNCTION, MECHANISMS, LESIONS

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MLA
Hoste, Esther, et al. “Caspase-14-Deficient Mice Are More Prone to the Development of Parakeratosis.” JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol. 133, no. 3, 2013, pp. 742–50, doi:10.1038/jid.2012.350.
APA
Hoste, E., Denecker, G., Gilbert, B., Van Nieuwerburgh, F., van der Fits, L., Asselbergh, B., … Declercq, W. (2013). Caspase-14-deficient mice are more prone to the development of parakeratosis. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 133(3), 742–750. https://doi.org/10.1038/jid.2012.350
Chicago author-date
Hoste, Esther, Geertrui Denecker, Barbara Gilbert, Filip Van Nieuwerburgh, Leslie van der Fits, Bob Asselbergh, Riet De Rycke, et al. 2013. “Caspase-14-Deficient Mice Are More Prone to the Development of Parakeratosis.” JOURNAL OF INVESTIGATIVE DERMATOLOGY 133 (3): 742–50. https://doi.org/10.1038/jid.2012.350.
Chicago author-date (all authors)
Hoste, Esther, Geertrui Denecker, Barbara Gilbert, Filip Van Nieuwerburgh, Leslie van der Fits, Bob Asselbergh, Riet De Rycke, Jean-Pierre Hachem, Dieter Deforce, Errol P Prens, Peter Vandenabeele, and Wim Declercq. 2013. “Caspase-14-Deficient Mice Are More Prone to the Development of Parakeratosis.” JOURNAL OF INVESTIGATIVE DERMATOLOGY 133 (3): 742–750. doi:10.1038/jid.2012.350.
Vancouver
1.
Hoste E, Denecker G, Gilbert B, Van Nieuwerburgh F, van der Fits L, Asselbergh B, et al. Caspase-14-deficient mice are more prone to the development of parakeratosis. JOURNAL OF INVESTIGATIVE DERMATOLOGY. 2013;133(3):742–50.
IEEE
[1]
E. Hoste et al., “Caspase-14-deficient mice are more prone to the development of parakeratosis,” JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol. 133, no. 3, pp. 742–750, 2013.
@article{3165065,
  abstract     = {{Caspase-14 is an important protease in the proper formation of a fully functional skin barrier. Newborn mice that are deficient in caspase-14 exhibit increased transepidermal water loss and are highly sensitive to UVB-induced photodamage. Decreased caspase-14 expression and incomplete caspase-14 processing in lesional psoriatic parakeratotic stratum corneum has been reported previously. In this study, we show that caspase-14-deficient skin frequently displays incompletely cornified cells in the transitional zone between the granular and the cornified layers, pointing to a delay in cornification. We also demonstrate that after challenge of epidermal permeability barrier function by repetitive acetone treatment, a higher incidence of large parakeratotic plaques was observed in caspase-14-deficient skin. Furthermore, caspase-14-deficient mice are more prone than control mice to the development of parakeratosis upon induction of psoriasis-like dermatitis by imiquimod treatment. These results glow that lack of caspase-14 expression predisposes to the development of parakeratosis and that caspase-14 ha an important role in keratinocyte; terminal differentiation and the maintenance of normal stratum corneum, especially in conditions causing epidermal hyperproliferation.}},
  author       = {{Hoste, Esther and Denecker, Geertrui and Gilbert, Barbara and Van Nieuwerburgh, Filip and van der Fits, Leslie and Asselbergh, Bob and De Rycke, Riet and Hachem, Jean-Pierre and Deforce, Dieter and Prens, Errol P and Vandenabeele, Peter and Declercq, Wim}},
  issn         = {{0022-202X}},
  journal      = {{JOURNAL OF INVESTIGATIVE DERMATOLOGY}},
  keywords     = {{KERATINOCYTES,EXPRESSION,INFLAMMATION,IMIQUIMOD,DEGRADATION,PSORIASIS,SKIN,WATER-LOSS,HUMAN EPIDERMIS,BARRIER FUNCTION,MECHANISMS,LESIONS}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{742--750}},
  title        = {{Caspase-14-deficient mice are more prone to the development of parakeratosis}},
  url          = {{http://dx.doi.org/10.1038/jid.2012.350}},
  volume       = {{133}},
  year         = {{2013}},
}

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