The adhesion modulating properties of tenascin-W

• Published in: International journal of biological sciences 2012-01, Vol.8 (2), p.187-194
• Main Authors: Brellier, Florence, Martina, Enrico, Chiquet, Matthias, Ferralli, Jacqueline, van der Heyden, Michael, Orend, Gertraud, Schittny, Johannes C, Chiquet-Ehrismann, Ruth, Tucker, Richard P
• Format: Article
• Language: English
• Subjects: Actins - metabolism; Actins - physiology; Animals; Cell Adhesion; Cell Culture Techniques; Cell Line; Cell Movement; Cells, Cultured; Fibronectins - metabolism; Fibronectins - pharmacology; Fibronectins - physiology; Gene Expression Regulation; Gene Knockout Techniques; Mice; Pseudopodia - physiology; Pseudopodia - ultrastructure; Short Research Communication; Tenascin - genetics; Tenascin - metabolism; Tenascin - pharmacology; Tenascin - physiology; Wound Healing - genetics
• ISSN: 1449-2288; 1449-2288
• DOI: 10.7150/ijbs.8.187

Tenascins are extracellular matrix glycoproteins associated with cell motility, proliferation and differentiation. Tenascin-C inhibits cell spreading by binding to fibronectin; tenascin-R and tenascin-X also have anti-adhesive properties in vitro. Here we have studied the adhesion modulating properties of the most recently characterized tenascin, tenascin-W. C2C12 cells, a murine myoblast cell line, will form broad lamellipodia with stress fibers and focal adhesion complexes after culture on fibronectin. In contrast, C2C12 cells cultured on tenascin-W fail to spread and form stress fibers or focal adhesion complexes, and instead acquire a multipolar shape with short, actin-tipped pseudopodia. The same stellate morphology is observed when C2C12 cells are cultured on a mixture of fibronectin and tenascin-W, or on fibronectin in the presence of soluble tenascin-W. Tenascin-W combined with fibronectin also inhibits the spreading of mouse embryo fibroblasts when compared with cells cultured on fibronectin alone. The similarity between the adhesion modulating effects of tenascin-W and tenascin-C in vitro led us to study the possibility of tenascin-W compensating for tenascin-C in tenascin-C knockout mice, especially during epidermal wound healing. Dermal fibroblasts harvested from a tenascin-C knockout mouse express tenascin-W, but dermal fibroblasts taken from a wild type mouse do not. However, there is no upregulation of tenascin-W in the dermis of tenascin-C knockout mice, or in the granulation tissue of skin wounds in tenascin-C knockout animals. Similarly, tenascin-X is not upregulated in early wound granulation tissue in the tenascin-C knockout mice. Thus, tenascin-W is able to inhibit cell spreading in vitro and it is upregulated in dermal fibroblasts taken from the tenascin-C knockout mouse, but neither it nor tenascin-X are likely to compensate for missing tenascin-C during wound healing.