title: Coordinate upregulation of tenascin C expression with degree of photodamage in human skin.
abstract: Tenascin C is a large extracellular matrix glycoprotein involved in morphogenesis and wound healing. The distribution and expression levels of tenascin were examined in photodamaged skin to investigate the hypothesis that photoaged skin displays characteristics of wound repair. In situ hybridization and semiquantitative immunohistochemistry were performed on paired skin biopsies from patients with varying levels of photodamage, using monoclonal antibodies and cRNA probes for tenascin and its large isoform. In sun-protected skin, tenascin protein was distributed adjacent to the dermoepidermal junction, usually sparsely and discontinuously; tenascin mRNA was detected in dermal fibroblasts and some keratinocytes. In photodamaged skin, tenascin protein was increased in proportion to the clinical level of photodamage (analysis of variance: P < 0.0001, n = 29). With increased photodamage, tenascin protein expression became continuous along the dermoepidermal junction, extending deeper into and sometimes throughout the papillary dermis; tenascin mRNA was detected throughout the epidermis. Large tenascin isoform protein and mRNA distribution mirrored that of pantenascin, suggesting that it may be the predominant species in photodamaged skin. There was no correlation between tenascin expression levels and age or sex, and no seasonal variation was noted. The results indicate that photodamaged skin demonstrates tenascin increases consistent with an early wound healing response. However, tenascin increases in photodamage appear to be permanent and may therefore interfere with effective repair of ultraviolet-induced damage. In conclusion, this study has shown that dermal tenascin expression increases in proportion to the degree of photodamage. In normal skin, the temporal and spatial patterns of tenascin expression during morphogenesis and tissue remodelling are crucial to their correct progression. In photoageing, the 'normal' control of tenascin expression seems to be abrogated.
authors.affiliation: Biosciences Group, Unilever Research, Colworth House, Sharnbrook, Bedford MK44 1LQ, U.K. wendy.filsell@unilever.com
authors.forename: W
authors.initials: W
authors.lastname: Filsell
authors.forename: S
authors.initials: S
authors.lastname: Rudman
authors.forename: G
authors.initials: G
authors.lastname: Jenkins
authors.forename: M R
authors.initials: MR
authors.lastname: Green
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D010787:Photosensitivity Disorders / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D013472:Sunlight / Q000009:adverse effects; D019063:Tenascin / Q000378:metabolism*; D015854:Up-Regulation; D014945:Wound Healing / Q000502:physiology*
chemical_list: D019063:Tenascin