Glycobiology Advance Access originally published online on October 19, 2007
Glycobiology 2008 18(1):20-27; doi:10.1093/glycob/cwm115
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Accelerated Proliferation and Abnormal Differentiation of Epidermal Keratinocytes in Endo-β-Galactosidase C Transgenic Mice
2 Division of Resources Life Science, United Graduate School of Agricultural Sciences; Tottori University, 4-101 Koyama-Minami, Tottori 680-8553, Japan
3 Animal Genome Research Unit, Division of Animal Science, National Institute of Agrobiological Sciences, 2 Ikenodai, Tsukuba, Ibaraki 305-0901, Japan
4 Department of Biological Science, Faculty of Life and Environmental Science, Shimane University, 1060 Nishikawatsu-cho, Matsue, Shimane 690-8504, Japan
5 Department of Health Science, Faculty of Psychological and Physical Sciences, Aichi Gakuin University; 12 Araike, Iwasaki-cho, Aichi 470-0195, Japan
1 To whom correspondence should be addressed: Tel: +81-852-32-6536; Fax: +81-852-32-6429; e-mail: tmatsu{at}life.shimane-u.ac.jp
Received on March 2, 2007; revised on September 27, 2007; accepted on October 5, 2007
Transgenic (TG) mice that have systemically expressed Endo-β-galactosidase C (EndoGalC) have rough and flaky skin. This skin phenotype is detectable around 5 days postnatal and becomes obscure by 2 weeks after birth. Their epidermis is thickened but the dermis and hair follicles are normal in structure. EndoGalC, which removes the terminal Gal
1-3Gal disaccharide (Gal epitope), was expressed in the epidermis of TG mice. GS-IB4 lectin staining showed that the Gal epitope did not exist in the epidermis in TG but existed in wild-type (WT) mice. In TG mice, N-acetylglucosamines were exposed by EndoGalC, which is detected using GS-II lectin. To understand the cause of the epidermal thickening and skin phenotype, we examined the proliferation and differentiation of kerationocytes. BrdU-pulse-labeling revealed that proliferating keratinocytes increased approximately three-fold in TG epidermis compared to WT one. In TG epidermis, the expression domain of cytokeratin 14 increased from 1–2 layers to 4–5 layers and co-expressed with cytokeratin 6 and 10 in the upper layers. The layers expressing involucrin and loricrin also increased but those expressing filaggrin and transglutaminase looked normal. The localization of E-cadherin was similar in both TG and WT mice. Although TG mice showed delayed development of the barrier function around 8 days postnatal, they acquired the function by 12 days after birth. These results suggest that the absence of the Gal epitope or the exposed N-acetylglucosamine terminal could play a critical role in the proliferation of basal keratinocytes and differentiation of them into the spinous cells in newborn mice.
Key words: abnormal differentiation / endo-β-galactosidase C / epidermal hyperproliferation / keratinocyte / transgenic mice
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