4.4 Article

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

Journal

WOUND REPAIR AND REGENERATION
Volume 17, Issue 3, Pages 326-339

Publisher

WILEY
DOI: 10.1111/j.1524-475X.2009.00480.x

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Funding

  1. Canadian Institutes of Health Research (CIHR)

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Integrin alpha v beta 6 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-beta 1 (TGF-beta 1) 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-beta 1 activity. Therefore, alpha v beta 6 integrin-mediated regulation of TGF-beta 1 activity may be involved in this process. To determine the function of alpha v beta 6 integrin in glucocorticoid-induced impaired wound healing, both beta 6 integrin-deficient (beta 6-/-) and wild-type mice were exposed to dexamethasone treatment. Multiple wound parameters, keratinocyte proliferation, inflammation, and TGF-beta 1 activation were assessed. Wound healing was significantly accelerated in the dexamethasone-treated beta 6-/- mice compared with the corresponding wild-type mice. The dexamethasone-treated beta 6-/- mice showed enhanced keratinocyte proliferation in both wound epithelium and hair follicles while the production of proinflammatory cytokines and TGF-beta 1 activation were reduced. Accelerated wound repair in the dexamethasone-treated beta 6-/- mice might be associated with the reduced antiproliferative and proinflammatory effects of TGF-beta 1. Inhibition of alpha v beta 6 integrin may provide a future target for treatment of impaired wound healing.

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