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Mice lacking β6 integrin in skin show accelerated wound repair in dexamethasone impaired wound healing model

Integrin αvβ6 is an epithelial‐specific receptor that is absent from the healthy epidermis but synthesized de novo during wound repair. However, its function in wound repair is unknown. Integrin‐mediated transforming growth factor‐β1 (TGF‐β1) activation is the main activation mechanism of this key cytokine in vivo. Impaired wound healing caused by glucocorticoids is a major clinical problem and is associated with a disturbed balance of TGF‐β1 activity. Therefore, αvβ6 integrin‐mediated regulation of TGF‐β1 activity may be involved in this process. To determine the function of αvβ6 integrin in glucocorticoid‐induced impaired wound healing, both β6 integrin‐deficient (β6−/−) and wild‐type mice were exposed to dexamethasone treatment. Multiple wound parameters, keratinocyte proliferation, inflammation, and TGF‐β1 activation were assessed. Wound healing was significantly accelerated in the dexamethasone‐treated β6−/− mice compared with the corresponding wild‐type mice. The dexamethasone‐treated β6−/− mice showed enhanced keratinocyte proliferation in both wound epithelium and hair follicles while the production of proinflammatory cytokines and TGF‐β1 activation were reduced. Accelerated wound repair in the dexamethasone‐treated β6−/− mice might be associated with the reduced antiproliferative and proinflammatory effects of TGF‐β1. Inhibition of αvβ6 integrin may provide a future target for treatment of impaired wound healing.