During cutaneous wound healing, basal keratinocytes migrate laterally
to cover the wound bed, whereas in an unwounded situation they move ve
rtically and differentiate to constitute the different layers of the e
pidermis. Many extracellular factors influence the behavior of these c
ells. The main ones are extracellular matrix molecules and cytokines p
resent in the dermoepidermal junction and/or in the wound bed. Some of
them such as collagens type I and IV, fibronectin and epidermal growt
h factor are known to induce basal keratinocyte migration. On the cont
rary, others, such as laminin, inhibit it. Molecules from the VIA-inte
grin family are receptors for many of these extracellular matrix molec
ules. As specific adhesion and signal transduction molecules, they pla
y a critical role in keratinocyte migration by allowing interactions b
etween the cell cytoskeleton and the macromolecules in the wound bed.
This type of interaction is commonly seen in all the models of cell mi
gration reviewed herein. These models try to explain the different mec
hanisms involved in basal keratinocyte migration. The translation of t
his phenomenon, at a light microscopic level is the extension of the l
amellipodia/fillopodia at the leading edge of the cell. Finally, we pr
esent some dinical applications of the cumulative knowledge published
in this field in basic science journals.