Aberrant integrin expression during epidermal wound healing and in psoriatic epidermis.

Abstract

We have examined integrin expression during the remodeling of the epidermis that takes place during wound healing, using a suction blister model in which the epidermis is detached from the dermis, leaving the basement membrane intact.By immuno- fluorescence microscopy, we found that the same integrin sub- units were expressed during wound healing as in normal epider- mis with very little change in the relative intensity or distribu- tion of staining at the leading edge of the migrating epidermis.However, at the time of wound closure, when the epidermis is still hyperproliferative, a2, a3, a6, and t3, were no longer con- fined to the basal layer, as in normal epidermis, but were also found in all the living suprabasal cell layers, coexpressed with the terminal differentiation markers involucrin, keratin 10, and keratin 16.Strong suprabasal staining for a, was also found in one specimen.4, which normally forms a heterodimer with a6, and a5 remained predominantly basal.Three of the integrin ligands, fibronectin, type IV collagen, and laminin, remained largely confined to the basement membrane zone and dermis.By 14 d after wounding, the integrins were once more restricted to the basal layer.Suprabasal integrin expression was also observed in involved psoriatic lesions.Thus, in two situations in which the epidermis is hyperproliferative, there is a failure to downregulate integrin expression on initiation of terminal dif- ferentiation.The functional consequences of this aberrant inte- grin expression remain to be explored.(J.Clin.Invest.1992.89:1892-1901.)Key words: hyperproliferation * extracellular matrix * cell migration * terminal differentiation keratinocytes fined to the basal layer: keratinocytes express aoilI, 0231, a3#1, a5/31, a634, and avi35 (4-10).a,#, is only weakly detected in epidermis and is not seen consistently in culture; the keratino- cyte a,#,1 ligand is unknown (7, 8).In cultured keratinocytes,