| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Journal of Pathology, Vol 139, 1143-1150, Copyright © 1991 by American Society for Investigative Pathology
REGULAR ARTICLES |
J Schalkwijk, PM Steijlen, IM van Vlijmen-Willems, B Oosterling, EJ Mackie and AA Verstraeten
Department of Dermatology, University Hospital Nijmegen, The Netherlands.
The extracellular matrix glycoprotein tenascin is sparsely distributed in normal human dermis. The authors have shown that in a number of skin diseases (psoriasis, skin tumors), tenascin expression is strongly increased. In this immunohistochemical study, using polyclonal and monoclonal antisera, we have tested the hypothesis that tenascin expression in vivo is linked to epidermal proliferation. Using the sellotape stripping model in normal human skin, which causes a rapid recruitment of keratinocytes into the cell cycle, induction of tenascin expression was found in the upper dermis within 24 hours after stripping. In contrast, in normoproliferative monogenic disorders of keratinization (X-linked recessive ichthyosis, autosomal dominant ichthyosis vulgaris, non-erythrodermic lamellar ichthyosis), no increase in tenascin expression was found compared with normal skin. These findings demonstrate a relationship between epidermal proliferation and metabolic alterations in the dermal compartment.
This article has been cited by other articles:
![]() |
C. Meltendorf, G. J. Burbach, J. Buhren, R. Bug, C. Ohrloff, and T. Deller Corneal Femtosecond Laser Keratotomy Results in Isolated Stromal Injury and Favorable Wound-Healing Response Invest. Ophthalmol. Vis. Sci., May 1, 2007; 48(5): 2068 - 2075. [Abstract] [Full Text] [PDF] |
||||
![]() |
V Koljonen, T Jahkola, E Tukiainen, G Granroth, C Haglund, and T Bohling Tenascin-C in primary Merkel cell carcinoma J. Clin. Pathol., March 1, 2005; 58(3): 297 - 300. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Schalkwijk, M. C. Zweers, P. M. Steijlen, W. B. Dean, G. Taylor, I. M. van Vlijmen, B. van Haren, W. L. Miller, and J. Bristow A Recessive Form of the Ehlers-Danlos Syndrome Caused by Tenascin-X Deficiency N. Engl. J. Med., October 18, 2001; 345(16): 1167 - 1175. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Mackie and R. Tucker The tenascin-C knockout revisited J. Cell Sci., January 11, 1999; 112(22): 3847 - 3853. [Abstract] [PDF] |
||||
![]() |
T. Jarvinen, L Jozsa, P Kannus, T. Jarvinen, M Kvist, T Hurme, J Isola, H Kalimo, and M Jarvinen Mechanical loading regulates tenascin-C expression in the osteotendinous junction J. Cell Sci., January 9, 1999; 112(18): 3157 - 3166. [Abstract] [PDF] |
||||
![]() |
C. S. Swindle, K. T. Tran, T. D. Johnson, P. Banerjee, A. M. Mayes, L. Griffith, and A. Wells Epidermal growth factor (EGF)-like repeats of human tenascin-C as ligands for EGF receptor J. Cell Biol., July 23, 2001; 154(2): 459 - 468. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. J. Hicke, C. Marion, Y.-F. Chang, T. Gould, C. K. Lynott, D. Parma, P. G. Schmidt, and S. Warren Tenascin-C Aptamers Are Generated Using Tumor Cells and Purified Protein J. Biol. Chem., December 21, 2001; 276(52): 48644 - 48654. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |