The adhesion modulating properties of tenascin-w

Brellier, Florence; Martina, Enrico; Chiquet, Matthias; Ferralli, Jacqueline; van der Heyden, Michael; Orend, Gertraud; Schittny, Johannes C; Chiquet-Ehrismann, Ruth; Tucker, Richard P (2012). The adhesion modulating properties of tenascin-w. International journal of biological sciences, 8(2), pp. 187-94. Lake Haven (Aus.): Ivyspring International 10.7150/ijbs.8.187

Full text not available from this repository. (Request a copy)

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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > School of Dental Medicine > Department of Orthodontics
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy > Functional Anatomy

UniBE Contributor:

Chiquet, Matthias and Schittny, Johannes

ISSN:

1449-2288

Publisher:

Ivyspring International

Language:

English

Submitter:

Eveline Carmen Schuler

Date Deposited:

04 Oct 2013 14:17

Last Modified:

25 Jan 2017 12:15

Publisher DOI:

10.7150/ijbs.8.187

PubMed ID:

22211116

Web of Science ID:

000301061100003

URI:

https://boris.unibe.ch/id/eprint/5120 (FactScience: 209838)

Actions (login required)

Edit item Edit item
Provide Feedback