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Sci Rep. 2018 Dec 19;8(1):17967. doi: 10.1038/s41598-018-36272-9.

Vinculin and the mechanical response of adherent fibroblasts to matrix deformation.

Author information

1
Department of Materials, ETH Zürich, 8093, Zürich, Switzerland.
2
Department of Mechanical Engineering and Materials Science, Yale University, New Haven, CT, 06511, USA.
3
Cardiovascular Research Center and Department of Medicine (Cardiology), Yale University School of Medicine, New Haven, CT, 06511, USA.
4
Department of Cell Biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands.
5
Departments of Cell Biology and Biomedical Engineering, Yale University, New Haven, CT, 06511, USA.
6
Department of Materials, ETH Zürich, 8093, Zürich, Switzerland. eric.dufresne@mat.ethz.ch.
7
Department of Mechanical Engineering and Materials Science, Yale University, New Haven, CT, 06511, USA. eric.dufresne@mat.ethz.ch.

Abstract

Cells respond to the mechanics of their environment. Mechanical cues include extracellular matrix (ECM) stiffness and deformation, which are primarily sensed through integrin-mediated adhesions. We investigated the impact of ECM deformation on cellular forces, measuring the time-evolution of traction forces of isolated mouse fibroblasts in response to stretch and release. Stretch triggered a marked increase of traction stresses and apparent stiffness. Expression of the focal adhesion protein vinculin not only increased baseline traction forces, but also increased dissipation of mechanical energy, which was correlated with the cells' failure to recover baseline traction forces after release of stretch.

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