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. 2016 Sep 27;6:33919. doi: 10.1038/srep33919

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Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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(a) Stress-strain space diagram for the matrix in the microtissues with schematics showing the relative deflections of the micropillars. Red indicates that the magnetic field is active. The moment of cell seeding is taken to be the zero stress and zero strain condition (Point A). As the microtissue matures, cell contraction compresses the matrix (Point B). Mechanical loading and unloading drives the matrix between points B and C, causing reversible stretching (lower right Inset). Treating microtissues with Triton X-100 lyses the cells placing the matrix under tension due to the outward stress exerted by the micropillars with no counterbalancing active cellular contraction (Point D). Applying the loading profile to Triton-treated microtissues drives the matrix to point E. However, they never fully recover to point D as the tension yield stress is exceeded (upper right Inset). (b–e) Illustrations of the state of the ECM during these processes, highlighting the shielding effects of the cells. (b) SMCs (black ovals) are dispersed throughout the cross-linked (orange circles) collagen ECM (dashed green lines) and bind with it at focal adhesion sites. The total magnitude of the cellular active contractility F_cell is represented by the red arrows. Contractile forces are directed towards the cells’ centers, and the SMCs act as nodes of contractility for the ECM network. Blue bar represents cell-cell mechanical linkages. (c) As the tissue is stretched through the application of an external force, tissue stress σ increases as does the levels of cellular force generation. Due to the active contractility of the cells, the collagen network is shielded from plastic deformation caused by this stress increase, and mainly deforms elastically. (d) Permeabilizing the cell membrane and lysing the cells through Triton X-100 treatment places the microtissue under tension due to the stress produced by the deflected micropillars (). (e) Applying an additional external stress σ causes irreversible changes in the ECM microstructure through fiber alignment and changes in crosslinking, leading to plastic deformation.

Inline graphic — (a) Stress-strain space diagram for the matrix in the microtissues with schematics showing the relative deflections of the micropillars. Red indicates that the magnetic field is active. The moment of cell seeding is taken to be the zero stress and zero strain condition (Point A). As the microtissue matures, cell contraction compresses the matrix (Point B). Mechanical loading and unloading drives the matrix between points B and C, causing reversible stretching (lower right Inset). Treating microtissues with Triton X-100 lyses the cells placing the matrix under tension due to the outward stress exerted by the micropillars with no counterbalancing active cellular contraction (Point D). Applying the loading profile to Triton-treated microtissues drives the matrix to point E. However, they never fully recover to point D as the tension yield stress is exceeded (upper right Inset). (b–e) Illustrations of the state of the ECM during these processes, highlighting the shielding effects of the cells. (b) SMCs (black ovals) are dispersed throughout the cross-linked (orange circles) collagen ECM (dashed green lines) and bind with it at focal adhesion sites. The total magnitude of the cellular active contractility F_cell is represented by the red arrows. Contractile forces are directed towards the cells’ centers, and the SMCs act as nodes of contractility for the ECM network. Blue bar represents cell-cell mechanical linkages. (c) As the tissue is stretched through the application of an external force, tissue stress σ increases as does the levels of cellular force generation. Due to the active contractility of the cells, the collagen network is shielded from plastic deformation caused by this stress increase, and mainly deforms elastically. (d) Permeabilizing the cell membrane and lysing the cells through Triton X-100 treatment places the microtissue under tension due to the stress produced by the deflected micropillars (). (e) Applying an additional external stress σ causes irreversible changes in the ECM microstructure through fiber alignment and changes in crosslinking, leading to plastic deformation.