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Epidermal deletion of HIF-2α stimulates wound closure.


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Authors

Cowburn, Andrew S 
Alexander, Laura E Crotty 
Southwood, Mark 
Nizet, Victor 
Chilvers, Edwin R 

Abstract

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.

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Keywords

Animals, Basic Helix-Loop-Helix Transcription Factors, Cell Hypoxia, Cell Line, Transformed, Dermatitis, Epidermal Cells, Epidermis, Female, Gene Deletion, Humans, Keratinocytes, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Von Hippel-Lindau Tumor Suppressor Protein, Wound Healing

Journal Title

J Invest Dermatol

Conference Name

Journal ISSN

0022-202X
1523-1747

Volume Title

134

Publisher

Elsevier BV
Sponsorship
National Cancer Institute (R01CA153983)
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)
This work was funded by Cambridge NIHR BRC, Papworth Hospital NHS trust, The Wellcome Trust (WT092738MA), and the National Institutes of Health (5R01AI093451).