Induction of tenascin in healing wounds.

Abstract

Abstract. The distribution of the extracellular matrix glycoprotein, tenascin, in normal skin and healing skin wounds in rats, has been investigated by immunohistochemistry. In normal skin, tenascin was sparsely distributed, predominantly in association with basement membranes. In wounds, there was a marked increase in the expression of tenascin at the wound edge in all levels of the skin. There was also particularly strong tenascin staining at the dermal-epidermal junction beneath migrating, proliferating epidermis. Tenascin was present throughout the matrix of the granulation tissue, which filled full-thickness wounds, but was not detectable in the scar after wound contraction was complete. The distribution of tenascin was spatially and temporally different from that of fibronectin, and tenascin appeared before laminin beneath migrating epidermis. Tenascin was not entirely codistributed with myofibroblasts, the contractile wound fibroblasts. In EM studies of wounds, tenascin was localized in the basal lamina at the dermalepidermal junction, as well as in the extracellular matrix of the adjacent dermal stroma, where it was either distributed homogeneously or bound to the surface of collagen fbers. In cultured skin explants, in which epidermis migrated over the cut edge of the dermis, tenascin, but not fibronectin, appeared in the dermis underlying the migrating epithelium. This demonstrates that migrating, proliferating epidermis induces the production of tenascin. The results presented here suggest that tenascin is important in wound healing and is subject to quite different regulatory mechanisms than is fibronectin.

Coregulation of Fibronectin Signaling and Matrix Contraction by Tenascin-C and Syndecan-4

“…Tenascin-C is highly expressed during tissue remodeling and repair (Jones and Jones, 2000;ChiquetEhrismann and Chiquet, 2003). Deposition of tenascin-C is markedly increased at the wound edges, particularly at the dermal-epidermal junction (Mackie et al, 1988). Its modulatory effects on cell adhesion suggest a role in promoting epidermal cell migration and proliferation.…”

Therapeutic Potential of Gingival Fibroblasts for Cutaneous Radiation Syndrome: Comparison to Bone Marrow-Mesenchymal Stem Cell Grafts

“…Our findings are thus in line with the report of tenascin-C involvement in myofibroblast recruitment [26]; the presence of tenascin-C on day 50 postirradiation in our study signals immature tissue granulation and on-going migration. MSC and GF treatment thus appear to have accelerated the wound healing process, with tenascin-C rapidly disappearing after wound contraction was complete [33]. The a-SMA + myofibroblasts are present in the early stage of the wound, and they rapidly disappear when wound healing progresses [34].…”

“…In the mice treated by MSCs and GFs, real-time PCR analysis showed that tenascin-C expression remained high compared to nonirradiated mice, but immunostaining revealed discontinuous localization in the dermal-epidermal junction, mostly close to hair follicles. Some reports indicate that tenascin-C is present throughout the matrix of granulation tissue, filling full-thickness wounds, but it is not detectable in the scar after the completion of wound contraction [33]. Tenascin-C may also interact with the contractile properties of myofibroblasts to influence wound contraction.…”

Mechanoregulation of gene expression in fibroblasts

“…The genes of focus in these studies are tenascin-C and collagen fibril-associated type XII collagen. Tenascin-C, which is not normally expressed in adults, changes its expression patterns during embryogenesis and regenerative processes and appears under pathological conditions and adjacent to contracting wounds (Mackie et al, 1988;Silver et al, 2003). Tensile loading has been shown to control tenascin-C mRNA expression in chicken skin fibroblasts.…”