Journal
CURRENT OPINION IN CELL BIOLOGY
Volume 12, Issue 5, Pages 554-562Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/S0955-0674(00)00131-9
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Funding
- NCI NIH HHS [CA49259] Funding Source: Medline
- NIAMS NIH HHS [AR21557] Funding Source: Medline
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Adhesion of keratinocytes in a wound outgrowth to laminin 5 in the basement membrane via integrins alpha 6 beta 4 and alpha 3 beta 1 is distinct from adhesion to dermal collagen via alpha 2 beta 1 or to fibronectin via alpha 5 beta 1. Leading cells in the outgrowth are distinguished from following keratinocytes by deposition of laminin 5, failure to communicate via gap junctions and sensitivity to toxin B, an inhibitor of RhoGTPase. Laminin 5 deposited by leading keratinocytes onto dermal collagen dominates over dermal ligands and changes the cell signals required for adhesion from collagen-dependent to laminin-5-dependent. Thus, deposition of laminin 5 can instruct keratinocytes to switch from an activated phenotype to a quiescent and integrated epithelial phenotype.
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