| First Author | Cowburn AS | Year | 2014 |
| Journal | J Invest Dermatol | Volume | 134 |
| Issue | 3 | Pages | 801-808 |
| PubMed ID | 24037341 | Mgi Jnum | J:206050 |
| Mgi Id | MGI:5547694 | Doi | 10.1038/jid.2013.395 |
| Citation | Cowburn AS, et al. (2014) Epidermal Deletion of HIF-2alpha Stimulates Wound Closure. J Invest Dermatol 134(3):801-8 |
| abstractText | 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-1alpha 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-2alpha. 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-2alpha response in keratinocytes could be a useful means to accelerate wound healing and tissue repair. |
