Abstract
Cutaneous wound healing is a complex process that ends with scar formation in adult skin. In contrast, fetal skin within the first and second trimesters of development heals without a scar. One of the most important aspects of scarless fetal wound repair appears to be the lack of inflammation in these wounds, suggesting that acute inflammation can promote scar formation in the skin. While it is well accepted that inflammation causes scar formation in the fetus, it is not known what specific factors produced during inflammation are responsible for these effects. The present experiments tested the possibility that oxidants released by activated inflammatory cells can contribute to scar tissue production by inducing inflammation in the fetus. Using a murine fetal wound repair model we demonstrate that hydrogen peroxide increased E15 (embryonic day 15) fibroblast proliferation and ultimately interfered with scarless healing in E15 skin, possibly through the induction of TGF-β1. Defining the factors produced during the inflammatory response that contribute to scar formation could be important for the development of new therapies designed to minimize adult scarring.
Published Version
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