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Comparative and Functional Genomics
Volume 4 (2003), Issue 1, Pages 47-55

Early Gene Expression in Wounded Human Keratinocytes Revealed by DNA Microarray Analysis

1Laboratoire de Physiologie Génomique des Eucaryotes, CNRS/UNSA UMR 6097, IPMC, F-06560 Sophia Antipolis, France
2Laboratoire de Biologie et Physiologie de la Peau, INSERM U385, Faculté de Médecine, Nice F-06107, France
3Laboratoire de Physiologie des Membranes Cellulaires, CNRS UMR6078 Bat. J. Maetz, Villefranche-sur-Mer, France
4Laboratoire de Physiologie Génomique des Eucaryotes, IPMC, 660, Route des Lucioles, Sophia Antipolis, Valbonne 06560, France

Received 13 September 2002; Accepted 21 November 2002

Copyright © 2003 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Wound healing involves several steps: spreading of the cells, migration and proliferation. We have profiled gene expression during the early events of wound healing in normal human keratinocytes with a home-made DNA microarray containing about 1000 relevant human probes. An original wounding machine was used, that allows the wounding of up to 40% of the surface of a confluent monolayer of cultured cells grown on a Petri dish (compared with 5% with a classical ‘scratch’ method). The two aims of the present study were: (a) to validate a limited number of genes by comparing the expression levels obtained with this technique with those found in the literature; (b) to combine the use of the wounding machine with DNA microarray analysis for large-scale detection of the molecular events triggered during the early stages of the wound-healing process. The time-courses of RNA expression observed at 0.5, 1.5, 3, 6 and 15 h after wounding for genes such as c-Fos, c-Jun, Egr1, the plasminogen activator PLAU (uPA) and the signal transducer and transcription activator STAT3, were consistent with previously published data. This suggests that our methodologies are able to perform quantitative measurement of gene expression. Transcripts encoding two zinc finger proteins, ZFP36 and ZNF161, and the tumour necrosis factor α-induced protein TNFAIP3, were also overexpressed after wounding. The role of the p38 mitogen-activated protein kinase (p38MAPK) in wound healing was shown after the inhibition of p38 by SB203580, but our results also suggest the existence of surrogate activating pathways.