Crimp length decreases in lax tendons due to cytoskeletal tension, but is restored with tensional homeostasis

The importance of tissue remodelling is widely accepted, but the mechanism by which the remodelling process occurs remains poorly understood. At the tissue scale, the concept of tensional homeostasis, in which there exists a target stress for a cell and remodelling functions to move the cell stress towards that target, is an important foundation for much theoretical work. We present here a theoretical model of a cell in parallel with a network to study what factors of the remodelling process help the cell move towards mechanical stability. The cell-network system was deformed and kept at constant stress. Remodelling was modelled by simulating strain-dependent degradation of collagen fibres and four different cases of collagen addition. The model did not lead to complete tensional homeostasis in the range of conditions studied, but it showed how different expressions for deposition and removal of collagen in a fibre network can interact to modulate the cell's ability to shield itself from an imposed stress by remodelling the surroundings. This study also showed how delicate the balance between deposition and removal rates is and how sensitive the remodelling process is to small changes in the remodelling rules.

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Chapter 6 Cell Optical Displacement Assay (CODA)—Measurements of Cytoskeletal Tension in Living Plant Cells with a Laser Optical Trap

Methods in Cell Biology ◽

10.1016/s0091-679x(08)61447-8 ◽

1995 ◽

pp. 71-84 ◽

Cited By ~ 6

Author(s):

Melvin Schindler

Keyword(s):

Optical Trap ◽

Plant Cells ◽

Living Plant ◽

Optical Displacement ◽

Cytoskeletal Tension ◽

Displacement Assay

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Tensional Homeostasis

Encyclopedia of Cancer ◽

10.1007/978-3-540-47648-1_5727 ◽

2008 ◽

pp. 2937-2940

Author(s):

Inkyung Kang ◽

Valerie M. Weaver

Keyword(s):

Tensional Homeostasis

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Tensional Homeostasis

10.1007/springerreference_177383 ◽

2012 ◽

Keyword(s):

Tensional Homeostasis

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Cell phenotypic plasticity requires autophagic flux driven by YAP/TAZ mechanotransduction

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1908228116 ◽

2019 ◽

Vol 116 (36) ◽

pp. 17848-17857 ◽

Cited By ~ 18

Author(s):

Antonio Totaro ◽

Qiuyu Zhuang ◽

Tito Panciera ◽

Giusy Battilana ◽

Luca Azzolin ◽

...

Keyword(s):

Physical Property ◽

Cell Types ◽

Autophagic Flux ◽

Downstream Effectors ◽

Cellular Mechanotransduction ◽

Cytoskeletal Tension ◽

Transcriptional Rewiring ◽

Different Cell Types ◽

Stem Cell State

Autophagy, besides ensuring energy metabolism and organelle renewal, is crucial for the biology of adult normal and cancer stem cells. However, it remains incompletely understood how autophagy connects to stemness factors and the nature of the microenvironmental signals that pattern autophagy in different cell types. Here we advance in these directions by reporting that YAP/TAZ transcriptionally control autophagy, being critical for autophagosomal degradation into autolysosomes. YAP/TAZ are downstream effectors of cellular mechanotransduction and indeed we found that cell mechanics, dictated by the physical property of the ECM and cytoskeletal tension, profoundly impact on autophagic flux in a YAP/TAZ-mediated manner. Functionally, by using pancreatic and mammary organoid cultures, we found that YAP/TAZ-regulated autophagy is essential in normal cells for YAP/TAZ-mediated dedifferentiation and acquisition of self-renewing properties. In tumor cells, the YAP/TAZ–autophagy connection is key to sustain transformed traits and for acquisition of a cancer stem cell state by otherwise more benign cells. Mechanistically, YAP/TAZ promote autophagic flux by directly promoting the expression of Armus, a RAB7-GAP required for autophagosome turnover and whose add-back rescues autophagy in YAP/TAZ-depleted cells. These findings expand the influence of YAP/TAZ mechanotransduction to the control of autophagy and, vice versa, the role of autophagy in YAP/TAZ biology, and suggest a mechanism to coordinate transcriptional rewiring with cytoplasmic restructuring during cell reprogramming.

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Mechanical stimulation of single cells by reversible host-guest interactions in 3D microscaffolds

Science Advances ◽

10.1126/sciadv.abc2648 ◽

2020 ◽

Vol 6 (39) ◽

pp. eabc2648

Author(s):

Marc Hippler ◽

Kai Weißenbruch ◽

Kai Richler ◽

Enrico D. Lemma ◽

Masaki Nakahata ◽

...

Keyword(s):

Single Cells ◽

Three Dimensional ◽

Stimuli Responsive ◽

Traction Forces ◽

Set Point ◽

Cellular Processes ◽

Laser Lithography ◽

Cross Links ◽

Tensional Homeostasis ◽

Myosin Motors

Many essential cellular processes are regulated by mechanical properties of their microenvironment. Here, we introduce stimuli-responsive composite scaffolds fabricated by three-dimensional (3D) laser lithography to simultaneously stretch large numbers of single cells in tailored 3D microenvironments. The key material is a stimuli-responsive photoresist containing cross-links formed by noncovalent, directional interactions between β-cyclodextrin (host) and adamantane (guest). This allows reversible actuation under physiological conditions by application of soluble competitive guests. Cells adhering in these scaffolds build up initial traction forces of ~80 nN. After application of an equibiaxial stretch of up to 25%, cells remodel their actin cytoskeleton, double their traction forces, and equilibrate at a new dynamic set point within 30 min. When the stretch is released, traction forces gradually decrease until the initial set point is retrieved. Pharmacological inhibition or knockout of nonmuscle myosin 2A prevents these adjustments, suggesting that cellular tensional homeostasis strongly depends on functional myosin motors.

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