Epidermal deletion of HIF-2α stimulates wound closure.
Wound closure requires a complex series of micro-environmentally influenced events. A key aspect of wound closure is the migration of keratinocytes across the open wound. It has been found previously that the response to hypoxia via the HIF-1α transcription factor is a key feature of wound closure. The need for hypoxic response is likely due to interrupted wound vasculature, as well as infection, and in this work we investigated the need for a highly related hypoxic response transcription factor, HIF-2α. This factor was deleted tissue specifically in mice, and the resulting mice were found to have an accelerated rate of wound closure. This is correlated with a reduced bacterial load and inflammatory response in these mice. This indicates that manipulating or reducing the HIF-2α response in keratinocytes could be a useful means to accelerate wound healing and tissue repair.
Wellcome Trust (092738/Z/10/Z)
National Institute of Allergy and Infectious Diseases (R56AI090863)
National Institute of Allergy and Infectious Diseases (R01AI096852)
National Institute of Allergy and Infectious Diseases (R01AI093451)
National Institute of Allergy and Infectious Diseases (R01AI060840)