JGM Bergboer, GS Tjabringa, M Kamsteeg, IMJJ van Vlijmen-Willems, D Rodijk-Olthuis, PAM Jansen, J-Y Thuret, M Narita, A Ishida-Yamamoto, PLJM Zeeuwen, J Schalkwijk
Journal name: 
Am J Pathol
Citation info: 
Deletion of the late cornified envelope (LCE) genes LCE3B and LCE3C has recently been identified as a risk factor for psoriasis. Expression of 16 LCE genes of LCE groups 1, 2, 3, 5, and 6 was examined in vivo and in vitro. Quantitative PCR demonstrated that moderate to high LCE expression was largely confined to skin and a few oropharyngeal tissues. Genes of the LCE3 group demonstrated increased expression in lesional psoriatic epidermis and were induced after superficial injury of normal skin, whereas expression of members of other LCE groups was down-regulated under these conditions. Immunohistochemistry and immunoelectron microscopy demonstrated that LCE2 protein expression was restricted to the uppermost granular layer and the stratum corneum. Stimulation of in vitro reconstructed skin by several psoriasis-associated cytokines resulted in induction of LCE3 members. The data suggest that LCE proteins of groups 1, 2, 5, and 6 are involved in normal skin barrier function, whereas LCE3 genes encode proteins involved in barrier repair after injury or inflammation. These findings may provide clues to the mechanistic role of LCE3B/C deletion in psoriasis.
Research group: 
Narita Group
E-pub date: 
01 Apr 2011
Users with this publication listed: 
Masashi Narita