TENASCIN EXPRESSION DURING WOUND-HEALING IN HUMAN SKIN

Citation
Ma. Latinhouwers et al., TENASCIN EXPRESSION DURING WOUND-HEALING IN HUMAN SKIN, Journal of pathology, 178(1), 1996, pp. 30-35
Citations number
39
Categorie Soggetti
Pathology
Journal title
ISSN journal
00223417
Volume
178
Issue
1
Year of publication
1996
Pages
30 - 35
Database
ISI
SICI code
0022-3417(1996)178:1<30:TEDWIH>2.0.ZU;2-D
Abstract
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.