ISSN: 1449-2288International Journal of Biological Sciences
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Int J Biol Sci 2012; 8(2):187-194. doi:10.7150/ijbs.8.187 This issue Cite
Short Research Communication
The Adhesion Modulating Properties of Tenascin-W
1. Friedrich Miescher Institute for Biomedical Research, Novartis Research Foundation, CH-4058 Basel, Switzerland.
2. University of Basel, Faculty of Science, CH-4056 Basel, Switzerland.
3. Department of Orthodontics and Dentofacial Orthopedics, University of Bern, CH-3010 Bern, Switzerland.
4. Inserm, U682, Strasbourg, F-67200 France, University Strasbourg, UMR-S682, Strasbourg F-67081, France.
5. Institute of Anatomy, University of Bern, CH-3000 Bern, Switzerland.
6. Department of Cell Biology and Human Anatomy, University of California at Davis, Davis, California 95616 USA.
* These authors contributed equally to this work.
Abstract
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.
Keywords: tenascin, extracellular matrix, fibronectin, wound healing, C2C12.
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