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

Esther Hoste UGent, Geertrui Denecker UGent, Barbara Gilbert UGent, Filip Van Nieuwerburgh UGent, Leslie van der Fits, Bob Asselbergh UGent, Riet De Rycke UGent, Jean-Pierre Hachem, Dieter Deforce UGent, Errol P Prens, et al. (2013) JOURNAL OF INVESTIGATIVE DERMATOLOGY. 133(3). p.742-750
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.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
KERATINOCYTES, EXPRESSION, INFLAMMATION, IMIQUIMOD, DEGRADATION, PSORIASIS, SKIN, WATER-LOSS, HUMAN EPIDERMIS, BARRIER FUNCTION
journal title
JOURNAL OF INVESTIGATIVE DERMATOLOGY
J. Invest. Dermatol.
volume
133
issue
3
pages
742 - 750
Web of Science type
Article
Web of Science id
000315008500022
JCR category
DERMATOLOGY
JCR impact factor
6.372 (2013)
JCR rank
1/61 (2013)
JCR quartile
1 (2013)
ISSN
0022-202X
DOI
10.1038/jid.2012.350
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
3165065
handle
http://hdl.handle.net/1854/LU-3165065
date created
2013-03-14 12:17:45
date last changed
2016-12-19 15:39:25
@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},
  keyword      = {KERATINOCYTES,EXPRESSION,INFLAMMATION,IMIQUIMOD,DEGRADATION,PSORIASIS,SKIN,WATER-LOSS,HUMAN EPIDERMIS,BARRIER FUNCTION},
  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},
}

Chicago
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): 742–750.
APA
Hoste, Esther, Denecker, G., Gilbert, B., Van Nieuwerburgh, F., van der Fits, L., Asselbergh, B., De Rycke, R., et al. (2013). Caspase-14-deficient mice are more prone to the development of parakeratosis. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 133(3), 742–750.
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.
MLA
Hoste, Esther, Geertrui Denecker, Barbara Gilbert, et al. “Caspase-14-deficient Mice Are More Prone to the Development of Parakeratosis.” JOURNAL OF INVESTIGATIVE DERMATOLOGY 133.3 (2013): 742–750. Print.