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First published online January 17, 2009


Journal of Cell Science 122, 205e (2009)
© The Company of Biologists Limited
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Integrin {alpha}3β1 runs interference


Figure 1

Wound healing in the skin requires migration and hyperproliferation of keratinocytes. Integrin {alpha}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 {alpha}3-integrin-null mice, which die during the neonatal period. Controversially, integrin {alpha}3β1 has also been independently reported to promote and inhibit keratinocyte migration in vitro. Arnoud Sonnenberg and colleagues (p. 278) now generate epidermis-specific {alpha}3-integrin-knockout mice to investigate the function of integrin {alpha}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 {alpha}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 {alpha}3-integrin-deficient keratinocytes migrate with increased velocity and persistence. The authors' results support a role for {alpha}3β1 integrin in inhibiting the directional migration of keratinocytes in vitro and wound re-epithelialisation in vivo.


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Related articles in JCS:

Integrin {alpha}3β1 inhibits directional migration and wound re-epithelialization in the skin
Coert Margadant, Karine Raymond, Maaike Kreft, Norman Sachs, Hans Janssen, and Arnoud Sonnenberg
JCS 2009 122: 278-288. [Abstract] [Full Text]  




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