| First Author | Hoste E | Year | 2013 |
| Journal | J Invest Dermatol | Volume | 133 |
| Issue | 3 | Pages | 742-50 |
| PubMed ID | 23014340 | Mgi Jnum | J:196479 |
| Mgi Id | MGI:5488561 | Doi | 10.1038/jid.2012.350 |
| Citation | Hoste E, et al. (2013) Caspase-14-deficient mice are more prone to the development of parakeratosis. J Invest Dermatol 133(3):742-50 |
| abstractText | 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 show that lack of caspase-14 expression predisposes to the development of parakeratosis and that caspase-14 has an important role in keratinocyte terminal differentiation and the maintenance of normal stratum corneum, especially in conditions causing epidermal hyperproliferation. |
