First published online January 17, 2009
Journal of Cell Science 122, 205e (2009)
© The Company of Biologists Limited
Integrin
3β1 runs interference
Wound healing in the skin requires migration and hyperproliferation of keratinocytes. Integrin
3β1, among other members of the integrin family, mediates the attachment of basal epidermal keratinocytes to the basement membrane, so its role in adult skin and wound healing is of interest. Complicating such studies, however, are
3-integrin-null mice, which die during the neonatal period. Controversially, integrin
3β1 has also been independently reported to promote and inhibit keratinocyte migration in vitro. Arnoud Sonnenberg and colleagues (p. 278) now generate epidermis-specific
3-integrin-knockout mice to investigate the function of integrin
3β1 in wound re-epithelialisation. These mice are viable, but display local inflammation, hair loss, basement-membrane duplication and microblistering at the dermal-epidermal junction; hemidesmosome assembly and keratinocyte differentiation are not impaired. In the absence of integrin
3β1 there is no change in keratinocyte proliferation, the distribution of other integrins and the deposition of basement-membrane proteins in the wound bed, but wound healing is faster, suggesting accelerated keratinocyte migration. Supporting in vitro evidence shows that
3-integrin-deficient keratinocytes migrate with increased velocity and persistence. The authors' results support a role for
3β1 integrin in inhibiting the directional migration of keratinocytes in vitro and wound re-epithelialisation in vivo.

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JCS 2009 122: 278-288.
[Abstract]
[Full Text]