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Article Dans Une Revue Journal of Investigative Dermatology Année : 2005

Disturbed epidermal structure in mice with temporally controlled fatp4 deficiency.

Thomas Herrmann
  • Fonction : Auteur
Hermann-Josef Gröne
  • Fonction : Auteur
Lutz Langbein
  • Fonction : Auteur
Iris Kaiser
  • Fonction : Auteur
Isabella Gosch
  • Fonction : Auteur
Ute Bennemann
  • Fonction : Auteur
Adrian Francis Stewart
  • Fonction : Auteur
Wolfgang Stremmel
  • Fonction : Auteur

Résumé

So far, little is known about the physiological role of fatty acid transport protein 4 (Fatp4, Slc27a4). Mice with a targeted disruption of the Fatp4 gene display features of a human neonatally lethal restrictive dermopathy with a hyperproliferative hyperkeratosis, a disturbed epidermal barrier, a flat dermal-epidermal junction, a reduced number of pilo-sebaceous structures, and a compact dermis, demonstrating that Fatp4 is necessary for the formation of the epidermal barrier. Because Fatp4 is widely expressed, it is unclear whether intrinsic Fatp4 deficiency in the epidermis alone can cause changes in the epidermal structure or whether the abnormalities observed are secondary to the loss of Fatp4 in other organs. To evaluate the functional role of Fatp4 in the skin, we generated a mouse line with Fatp4 deficiency inducible in the epidermis. Mice with epidermal keratinocyte-specific Fatp4 deficiency developed a hyperproliferative hyperkeratosis with a disturbed epidermal barrier. These changes resemble the histological abnormalities in the epidermis of newborn mice with total Fatp4 deficiency. We conclude that Fatp4 in epidermal keratinocytes is essential for the maintenance of a normal epidermal structure.

Dates et versions

hal-00187551 , version 1 (14-11-2007)

Identifiants

Citer

Thomas Herrmann, Hermann-Josef Gröne, Lutz Langbein, Iris Kaiser, Isabella Gosch, et al.. Disturbed epidermal structure in mice with temporally controlled fatp4 deficiency.. Journal of Investigative Dermatology, 2005, 125 (6), pp.1228-35. ⟨10.1111/j.0022-202X.2005.23972.x⟩. ⟨hal-00187551⟩
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