β-catenin and transforming growth factor β have distinct roles regulating fibroblast cell motility and the induction of collagen lattice contractionReport as inadecuate




β-catenin and transforming growth factor β have distinct roles regulating fibroblast cell motility and the induction of collagen lattice contraction - Download this document for free, or read online. Document in PDF available to download.

BMC Cell Biology

, 10:38

First Online: 11 May 2009Received: 13 October 2008Accepted: 11 May 2009

Abstract

Backgroundβ-catenin and transforming growth factor β signaling are activated in fibroblasts during wound healing. Both signaling pathways positively regulate fibroblast proliferation during this reparative process, and the effect of transforming growth factor β is partially mediated by β-catenin. Other cellular processes, such as cell motility and the induction of extracellular matrix contraction, also play important roles during wound repair. We examined the function of β-catenin and its interaction with transforming growth factor β in cell motility and the induction of collagen lattice contraction.

ResultsFloating three dimensional collagen lattices seeded with cells expressing conditional null and stabilized β-catenin alleles, showed a modest negative relationship between β-catenin level and the degree of lattice contraction. Transforming growth factor β had a more dramatic effect, positively regulating lattice contraction. In contrast to the situation in the regulation of cell proliferation, this effect of transforming growth factor β was not mediated by β-catenin. Treating wild-type cells or primary human fibroblasts with dickkopf-1, which inhibits β-catenin, or lithium, which stimulates β-catenin produced similar results. Scratch wound assays and Boyden chamber motility studies using these same cells found that β-catenin positively regulated cell motility, while transforming growth factor β had little effect.

ConclusionThis data demonstrates the complexity of the interaction of various signaling pathways in the regulation of cell behavior during wound repair. Cell motility and the induction of collagen lattice contraction are not always coupled, and are likely regulated by different intracellular mechanisms. There is unlikely to be a single signaling pathway that acts as master regulator of fibroblast behavior in wound repair. β-catenin plays dominant role regulating cell motility, while transforming growth factor β plays a dominant role regulating the induction of collagen lattice contraction.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2121-10-38 contains supplementary material, which is available to authorized users.

Download fulltext PDF



Author: Raymond Poon - Saeid Amini Nik - Jessica Ahn - Laura Slade - Benjamin A Alman

Source: https://link.springer.com/article/10.1186/1471-2121-10-38



DOWNLOAD PDF




Related documents