FASEB J. Pierce now sold as Thermo Scientific
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
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 Email this article to a friend
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 reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jaakkola, P.
Right arrow Articles by Jalkanen, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jaakkola, P.
Right arrow Articles by Jalkanen, M.
(The FASEB Journal. 1998;12:959-969.)
© 1998 FASEB

RESEARCH COMMUNICATION

Wound reepithelialization activates a growth factor-responsive enhancer in migrating keratinocytes

Panu Jaakkolaa, Sirpa Kontusaarib, Tuire Kauppib, Arto Määttä1,a, and Markku Jalkanena,1

a Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, BioCity, FIN-20520 Turku, Finland
b Biocenter Oulu and Department of Biochemistry, University of Oulu, Linnanmaa, FIN-90571 Oulu, Finland

Wound reepithelialization and keratinocyte migration require strictly ordered gene expression, which is assumed to be initiated by locally released mitogens and exposure of the cells to different matrix components. The mechanisms triggering gene expression specifically during reepithelialization are poorly understood. The far upstream AP-1-driven, FGF-inducible response element (FiRE) of the syndecan-1 gene was activated during cutaneous wound healing in transgenic mice. FiRE was induced selectively in migrating but not in proliferating keratinocytes at the wound edge. The activation was initiated at the start of the cell migration, was persistent throughout the merging and stratification phases, and was terminated after completion of reepithelialization. Although FiRE has been found within the gene of syndecan-1, the proximal promoter of syndecan-1 was not required for activation of FiRE in the migrating keratinocytes. The wounding induced activation was inhibited by blocking cell surface growth factor receptors with suramin. However, the activation of FiRE in resting skin required simultaneous growth factor- and stress-induced signals, but could also be elicited by the phosphatase inhibitor, okadaic acid. The activation by both wounding and chemical stimuli was blocked by inhibiting extracellular regulated kinase and p38 MAP kinases, suggesting the involvement of at least two parallel signal transduction pathways in wounding induced gene activation. As FiRE shows specificity for migrating keratinocytes only, it can be a useful tool for future wound healing studies and for targeting genes to injured tissues.—Jaakkola, P., Kontusaari, S., Kauppi, T., Määttä, A., Jalkanen, M. FASEB J. 12, 959–969 (1998)


Key Words: EGF • FiRE • migration • syndecan-1 • TGF-{alpha} • transcription




This article has been cited by other articles:


Home page
 Mol. Endocrinol.Home page
Y. Zhang, K. McKeehan, Y. Lin, J. Zhang, and F. Wang
Fibroblast Growth Factor Receptor 1 (FGFR1) Tyrosine Phosphorylation Regulates Binding of FGFR Substrate 2{alpha} (FRS2{alpha}) But Not FRS2 to the Receptor
Mol. Endocrinol., January 1, 2008; 22(1): 167 - 175.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
O. Okamoto, S. Bachy, U. Odenthal, J. Bernaud, D. Rigal, H. Lortat-Jacob, N. Smyth, and P. Rousselle
Normal Human Keratinocytes Bind to the {alpha}3LG4/5 Domain of Unprocessed Laminin-5 through the Receptor Syndecan-1
J. Biol. Chem., November 7, 2003; 278(45): 44168 - 44177.
[Abstract] [Full Text] [PDF]

Home page
 J. Dent. Res.Home page
J. Rautava, T. Soukka, K. Heikinheimo, P.J. Miettinen, R.-P. Happonen, and P. Jaakkola
Different Mechanisms of Syndecan-1 Activation through a Fibroblast-growth-factor-inducible Response Element (FiRE) in Mucosal and Cutaneous Wounds
J. Dent. Res., May 1, 2003; 82(5): 382 - 387.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
J. Jameson, K. Ugarte, N. Chen, P. Yachi, E. Fuchs, R. Boismenu, and W. L. Havran
A Role for Skin gamma delta T Cells in Wound Repair
Science, April 26, 2002; 296(5568): 747 - 749.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Rousseau, F. Houle, H. Kotanides, L. Witte, J. Waltenberger, J. Landry, and J. Huot
Vascular Endothelial Growth Factor (VEGF)-driven Actin-based Motility Is Mediated by VEGFR2 and Requires Concerted Activation of Stress-activated Protein Kinase 2 (SAPK2/p38) and Geldanamycin-sensitive Phosphorylation of Focal Adhesion Kinase
J. Biol. Chem., March 31, 2000; 275(14): 10661 - 10672.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Maatta, P. Jaakkola, and M. Jalkanen
Extracellular Matrix-dependent Activation of Syndecan-1 Expression in Keratinocyte Growth Factor-treated Keratinocytes
J. Biol. Chem., April 2, 1999; 274(14): 9891 - 9898.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Maatta, C. Ruhrberg, and F. M. Watt
Structure and Regulation of the Envoplakin Gene
J. Biol. Chem., June 23, 2000; 275(26): 19857 - 19865.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J. Laferriere, F. Houle, M. M. Taher, K. Valerie, and J. Huot
Transendothelial Migration of Colon Carcinoma Cells Requires Expression of E-selectin by Endothelial Cells and Activation of Stress-activated Protein Kinase-2 (SAPK2/p38) in the Tumor Cells
J. Biol. Chem., August 31, 2001; 276(36): 33762 - 33772.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1998 by The Federation of American Societies for Experimental Biology.