<p>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.</p> <p>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 <italic>c-Fos, c-Jun, Egr1</italic>, 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.</p>
[]
Comp Funct Genomics. 2003 Feb; 4(1):47-55