In adult human skin, the expression of the extracellular matrix glycop
rotein tenascin is limited, Under hyperproliferative conditions such a
s psoriasis and epidermal tumours, dermal tenascin expression is stron
gly upregulated, The aim of this study was to investigate the pattern
and kinetics of tenascin expression in human skin during wound healing
and to address the question of whether keratinocytes can directly int
eract with tenascin during re-epithelialization. Tenascin expression w
as investigated in excisional mounds in normal human skin, in explants
of normal human skin, and in chronic venous ulcers, using immunohisto
chemistry. No tenascin staining was found directly underneath the lead
ing edge of the sheet of migrating keratinocytes in the excisional mou
nds and explants, In the excisional wounds and the ulcers, dermal tena
scin was strongly upregulated in areas adjacent to hyperproliferative
epidermis, These hyperproliferative areas are located approximately 10
-50 cells behind the leading edge, as assessed by staining for the Ki-
67 antigen and the proliferating cell nuclear antigen (PCNA). At the l
ater stages of normal mound healing and in the chronic ulcers, tenasci
n was also detected in the wound bed. In these areas, the dermal-epide
rmal junction stained positive for laminin but was negative for hepara
n sulphate, The absence of the latter basement membrane component sugg
ests that the formation of a new basement membrane is not completed in
these wounds, These findings suggest that tenascin is not a substrate
for migrating keratinocytes; that the rapid induction of tenascin exp
ression in the papillary dermis during mound healing results from inte
raction with the hyperproliferative epidermis; and that in the later s
tages of wound healing, keratinocytes can potentially interact with te
nascin in the wound bed, because the basement membrane of the neo-epid
ermis is incomplete.