Recent studies have shown that low concentrations of H2O2 are produced endogenously by nonphagocytes after wounding. We observed that H2O2 at such concentrations can stimulate proliferation as well as migration of keratinocytes in a scratch-wound assay. Both wounding and H2O2 can induce phosphorylation of ERK1/2 via EGFR, but the activation of ERK1/2 by H2O2 is more sustained and can last more than 8h. Sustained ERK1/2 activation is required for the increased proliferation and migration induced by H2O2. The p38 MAPK was also found to be phosphorylated upon treatment with H2O2 but it was not required for H2O2-induced migration or proliferation. Furthermore, it was observed that there is a cross talk between the ERK1/2 and the p38 pathways whereby inhibition of either pathway can lead to activation of the other. As a result, the motogenic effects of H2O2 were further enhanced when p38 was inhibited. Our data are consistent with the view that H2O2 may play an important signaling role in wound healing.
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