Integrin α3β1 inhibits directional migration and wound re-epithelialization in the skin

• DOI: 10.1242/jcs.029108
• Publication Date: 2008-12-31T18:24:22Z
• Authors: Coert Margadant; Karine Raymond; Maaike Kreft; Norman Sachs; Hans Janssen; Arnoud Sonnenberg
• Keywords: Hemidesmosome; Epidermis (zoology)

Re-epithelialization after skin wounding requires both migration and hyperproliferation of keratinocytes. Laminin-332 is deposited during over the provisional matrix. To investigate function laminin-332 binding integrin alpha3beta1 in wound re-epithelialization, we generated Itga3flox/flox; K14-Cre mice lacking alpha3 subunit specifically basal layer epidermis. These are viable but display several defects, including local inflammation, hair loss, basement membrane duplication microblistering at dermal-epidermal junction, whereas hemidesmosome assembly keratinocyte differentiation not impaired. Wound healing slightly faster absence alpha3beta1, proliferation, distribution other integrins deposition proteins bed unaltered. In vitro, cell spreading rescued by increased surface expression alpha6beta1 alpha3. The alpha3-deficient keratinocytes migrate with an velocity persistence, growth factor signaling, assembly, appeared to be normal. We suggest that delays newly on bed.