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First published online December 31, 2008
doi: 10.1242/10.1242/jcs.029108
Research Article |
3β1 inhibits directional migration and wound re-epithelialization in the skin
Division of Cell Biology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands
Author for correspondence (e-mail: a.sonnenberg{at}nki.nl)
Accepted 30 September 2008
Re-epithelialization after skin wounding requires both migration and hyperproliferation of keratinocytes. Laminin-332 is deposited during migration over the provisional matrix. To investigate the function of the laminin-332 binding integrin 
3β1 in wound re-epithelialization, we generated Itga3flox/flox; K14-Cre mice lacking the 3 subunit specifically in the basal layer of the epidermis. These mice are viable but display several skin defects, including local inflammation, hair loss, basement membrane duplication and microblistering at the dermal-epidermal junction, whereas hemidesmosome assembly and keratinocyte differentiation are not impaired. Wound healing is slightly faster in the absence of integrin 3β1, whereas proliferation, the distribution of other integrins and the deposition of basement membrane proteins in the wound bed are unaltered. In vitro, cell spreading is rescued by increased surface expression of 6β1 integrin in the absence of integrin 3. The 3-deficient keratinocytes migrate with an increased velocity and persistence, whereas proliferation, growth factor signaling, hemidesmosome assembly, and laminin-332 deposition appeared to be normal. We suggest that integrin 3β1 delays keratinocyte migration during wound re-epithelialization, by binding to the laminin-332 that is newly deposited on the wound bed.
Key words: Integrin, Keratinocyte, Laminin-5, Migration, Wound healing
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