Dermo-epidermal separation is associated with induced tenascin expression in human skin

Abstract

Tenascin, a large glycoprotein of the extracellular matrix, shows a site-restricted distribution during embryogenesis. and can be found in adults in a variety of pathological conditions. In normal skin, tenascin is expressed at low levels, but it is upregulated in skin tumours, in a number of skin diseases with epidermal hyperproliferation and during wound healing. Several tenascin variants have been described, and these arise by alternative splicing. Using a monoclonal antibody recognizing all tenascin variants, and polyclonal antibodies specific for the large tenascin variants, we have investigated tenascin expression in bullous diseases such as epidermoiysis bullosa. pemphigus, bullous pemphigoid and pemphigoid gestationis. By immunohistochemistry. we have found increased tenascin staining in all patient skin samples, with a more pronounced tenascin expression in samples of autoimmune bullous diseases. The large tenascin variants seem to be major forms of tenascin occurring in healthy skin. In patients with blistering diseases, however, these large variants appear to represent a subpopulation of the induced tenascin accumulation. These findings suggest different functions for the tenascin variants in normal and diseased skin.

Cleavage of extracellular matrix in periodontitis: Gingipains differentially affect cell adhesion activities of fibronectin and tenascin-C

“…After a blocking step in 1% milk, membranes were incubated with rabbit polyclonal anti-fibronectin antibody (1:500) [35], mouse monoclonal antibody B28-13 raised against the constant C-terminal domain of human tenascin-C (1:200) [36], mouse monoclonal antibody C18-13 against the alternatively spliced domain of tenascin-C (1:100), or mouse anti-his antibody (1:100, Quiagen, Switzerland). They were then incubated for 1 h with anti-rabbit or anti-mouse IgG coupled to horseradish peroxidase (1:2000; Jackson ImmunoResearch, Suffolk, UK).…”

Induction of phenotype modifying cytokines by FERMT1 mutations

“…In KS, the inflammation seems to have two components: on one hand, the secretion of cytokines by kindlin-1 null keratinocytes and, on the other hand, the infiltration with macrophages. The massive upregulation of tenascin C, which is not seen in normal skin (Schenk, et al, 1995), is likely to reflect continuous tissue and basement membrane remodelling processes in KS. It is difficult to establish the precise contribution of each pathogenic factor.…”

Tenascin-W is a better cancer biomarker than tenascin-C for most human solid tumors

“…These tumor samples can be compared to the healthy skin tissue shown in Figure 3E. TNW was not detectable in any normal skin sample whereas TNC was observed in the dermis of three out of six samples (Figure 3D), just below the basement membrane underlying the basal epidermal cell layer, as has been described previously [21]. A summary of all stainings is presented in a table (Figure 3D).…”