TENASCIN EXPRESSION DURING WOUND HEALING IN HUMAN SKIN

✍ Scribed by LATIJNHOUWERS, MIEKE A.; BERGERS, MIEKE; VAN BERGEN, BERT H.; SPRUIJT, KARIN I.; ANDRIESSEN, MONIQUE P.; SCHALKWIJK, JOOST

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 769 KB
• Volume: 178
• Category: Article
• ISSN: 0022-3417
• DOI: 10.1002/(sici)1096-9896(199601)178:1<30::aid-path442>3.0.co;2-7

✦ Synopsis

In adult human skin, the expression of the extracellular matrix glycoprotein tenascin is limited. Under hyperproliferative conditions such as psoriasis and epidermal tumours, dermal tenascin expression is strongly 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 interact with tenascin during re-epithelialization. Tenascin expression was investigated in excisional wounds in normal human skin, in explants of normal human skin, and in chronic venous ulcers, using immunohistochemistry. No tenascin staining was found directly underneath the leading edge of the sheet of migrating keratinocytes in the excisional wounds and explants. In the excisional wounds and the ulcers, dermal tenascin 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 later stages of normal wound healing and in the chronic ulcers, tenascin was also detected in the wound bed. In these areas, the dermal-epidermal junction stained positive for laminin but was negative for heparan sulphate. The absence of the latter basement membrane component suggests 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 expression in the papillary dermis during wound healing results from interaction with the hyperproliferative epidermis; and that in the later stages of wound healing, keratinocytes can potentially interact with tenascin in the wound bed, because the basement membrane of the neo-epidermis is incomplete.