Glycobiology Advance Access published online on October 19, 2007
Glycobiology, doi:10.1093/glycob/cwm115
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Accelerated Proliferation And Abnormal Differentiation of Epidermal Keratinocytes in Endo-ß-Galactosidase C Transgenic Mice
1 Division of Resources Life Science, United Graduate School of Agricultural Sciences; Tottori University, 4-101 Koyama-Minami, Tottori 680-8553, Japan
2 Animal Genome Research Unit, Division of Animal Science, National Institute of Agrobiological Sciences, 2 Ikenodai, Tsukuba, Ibaraki 305-0901, Japan
3 Department of Biological Science, Faculty of Life and Environmental Science, Shimane University, 1060 Nishikawatsu-cho, Matsue, Shimane 690-8504, Japan
4 Department of Health Science, Faculty of Psychological and Physical Sciences, Aichi Gakuin University; 12 Araike, Iwasaki-cho, Aichi 470-0195, Japan
* To whom correspondence should be addressed: Takashi Matsuzaki Department of Biological Science, Faculty of Life and Environmental Science, Shimane University, 1060 Nishikawatsu-cho, Matsue, Shimane 690-8504, Japan Tel: +81-852-32-6536; Fax: +81-852-32-6429; e-mail: tmatsu{at}life.shimane-u.ac.jp
Received on March 2, 2007; accepted on October 5, 2007
Transgenic (TG) mice that have systemically expressed Endo-ß-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-ß-galactosidase C / epidermal hyperproliferation / keratinocyte / transgenic mice
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  R. Uematsu, Y. Shinohara, H. Nakagawa, M. Kurogochi, J.-i. Furukawa, Y. Miura, M. Akiyama, H. Shimizu, and S.-I. Nishimura Glycosylation Specific for Adhesion Molecules in Epidermis and Its Receptor Revealed by Glycoform-focused Reverse Genomics Mol. Cell. Proteomics, February 1, 2009; 8(2): 232 - 244. [Abstract] [Full Text] [PDF]
|
|