Fate of migrating epidermal cells during the wound healing using the injured-epithelia specific gene recombination.

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Injury to the skin tissue elicits an acute repair response aimed at restoring the epithelial continuity, which is essential to a normal skin barrier function. Epidermal keratinocytes at the wound edge are recruited for the re-epithelialization of the wound site. However, the mechanism of the re-epithelialization of the stratified epithelia is not easily understood compared with that of the simple epithelia. While the migration of keratinocytes occurs in the form of a stratified sheet at the wound edge, the relative contribution and ultimate fate of progenitor and differentiating keratinocytes during this vital process remains unclear. In this study, we used the transgenic technology to induce the wound specific gene recombination. We prepared two types of transgenes to introduce the injured epidermis specific gene modification and to induce the injured-suprabasal keratinocytes specific gene marking. One construct aimed to express the cre recombinase with the injured keratinocytes specific manner under the human keratin 6 promoter, and the other one was used for gene marking using the double marker proteins, GFP and galactosidase, We used the double transgenic mice to trace the migration of the suprabasal keratinocytes activated at the wound edge. By this transgenic work we could conclude the long term question, whether the suprabasal keratinocytes could recover the mitogenic property and migrate into the ulcerative surface or not. The suprabasal keratinocytes at the wound edge are possible to migrate into the ulcerative surfaces but never recover the mitotic activity even after the re-epithelialization.