CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jensen, P. J.
Right arrow Articles by Lavker, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jensen, P. J.
Right arrow Articles by Lavker, R. M.

Cell Growth & Differentiation, Vol 7, Issue 12 1793-1804, Copyright © 1996 by American Association of Cancer Research


ARTICLES

Modulation of the plasminogen activator cascade during enhanced epidermal proliferation in vivo

PJ Jensen and RM Lavker
Department of Dermatology, University of Pennsylvania School of Medicine, Philadelphia 19104-6142, USA.

Many lines of evidence support an involvement of urokinase plasminogen activator (uPA) and its type 1 inhibitor (PAI-1) in the migration of a variety of cells, including normal keratinocytes and carcinoma lines. In the present study, uPA expression was found to be a characteristic not just of migratory but also of proliferative keratinocytes. A variety of naturally occurring and experimentally induced epidermal hyperproliferative conditions were examined in mice, including fetal and neonatal epidermis, tape-stripped epidermis, and epidermis from which the hairs had been gently plucked. In all cases, epidermal hyperproliferation was accompanied by elevated levels of uPA mRNA (as measured by in situ hybridization) and activity (as measured by zymography). uPA mRNA was predominantly localized in the basal and immediately suprabasal cells, which constitute the proliferative population. To determine whether a PAI was concomitantly elevated, in situ hybridization for PAI-1 and PAI-2 was performed. PAI-2 but not PAI-1 mRNA was detected in fetal and neonatal epidermis, localized in the spinous layers. Although mRNAs for both inhibitors were induced by tape-stripping or hair-plucking, their distribution was more focal and more transient than that of uPA mRNA. These findings show that uPA, but not its usual inhibitors, is consistently elevated in the proliferative population of keratinocytes in a diverse range of hyperproliferative states. Two hypotheses are suggested by these data: (a) uPA may play a regulatory role in the activation of epidermal proliferation; or (b) uPA may be involved in the vertical migration of keratinocytes that must accompany increased cell proliferation.


This article has been cited by other articles:


Home page
J. Cell Sci.Home page
K. M. Providence, L. A. White, J. Tang, J. Gonclaves, L. Staiano-Coico, and P. J. Higgins
Epithelial monolayer wounding stimulates binding of USF-1 to an E-box motif in the plasminogen activator inhibitor type 1 gene
J. Cell Sci., October 1, 2002; 115(19): 3767 - 3777.
[Abstract] [Full Text] [PDF]


Home page
IOVSHome page
D. L. Williams, B. Risse, S. Kim, D. Saunders, S. Orlin, M. S. Baker, P. J. Jensen, and R. M. Lavker
Plasminogen Activator Inhibitor Type 2 in Human Corneal Epithelium
, July 1, 1999; 40(8): 1669 - 1675.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
A. A.-R. Higazi, K. Bdeir, E. Hiss, S. Arad, A. Kuo, I. Barghouti, and D. B. Cines
Lysis of Plasma Clots by Urokinase-Soluble Urokinase Receptor Complexes
Blood, September 15, 1998; 92(6): 2075 - 2083.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1996 by the American Association of Cancer Research.