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- W2044292027 abstract "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." @default.
- W2044292027 created "2016-06-24" @default.
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- W2044292027 date "2009-05-01" @default.
- W2044292027 modified "2023-10-14" @default.
- W2044292027 title "Mice lacking β6 integrin in skin show accelerated wound repair in dexamethasone impaired wound healing model" @default.
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- W2044292027 doi "https://doi.org/10.1111/j.1524-475x.2009.00480.x" @default.
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