Vimentin intermediate filaments modulate cell traction force but not cell sensitivity to substrate stiffness

Cytoskeleton ◽  
2021 ◽  
Author(s):  
Minh‐Tri Ho Thanh ◽  
Allie Grella ◽  
Denis Kole ◽  
Sakthikumar Ambady ◽  
Qi Wen
Keyword(s):  
Intermediate Filaments ◽  
Traction Force ◽  
Substrate Stiffness ◽  
Cell Sensitivity ◽  
Cell Traction

scholarly journals Does cellular adaptation to force loading rate determine the biphasic vs monotonic response of actin retrograde flow with substrate rigidity?

2021 ◽  
Author(s):  
Partho Sakha De ◽  
Rumi De
Keyword(s):  
Cancer Progression ◽  
Loading Rate ◽  
Focal Adhesions ◽  
Traction Force ◽  
Leading Edge ◽  
Substrate Stiffness ◽  
Retrograde Flow ◽  
Force Loading ◽  
Substrate Rigidity ◽  
Cell Traction

AbstractThe transmission of cytoskeletal forces to the extracellular matrix through focal adhesion complexes is essential for a multitude of biological processes such as cell migration, differentiation, tissue development, cancer progression, among others. During migration, focal adhesions arrest the actin retrograde flow towards the cell interior, allowing the cell front to move forward. Here, we address a puzzling observation of the existence of two distinct phenomena: a biphasic relationship of the retrograde flow and cell traction force with increasing substrate rigidity, with maximum traction force and minimum retrograde flow velocity being present at an optimal substrate stiffness; in contrast, a monotonic relationship between them where the retrograde flow decreases and traction force increases with substrate stiffness. We propose a theoretical model for cell-matrix adhesions at the leading edge of a migrating cell, incorporating a novel approach in force loading rate sensitive binding and reinforcement of focal adhesions assembly and the subsequent force-induced slowing down of actin flow. Our model unravels both biphasic and monotonic responses of the retrograde flow and cell traction force with increasing substrate rigidity, owing to the cell’s ability to sense and adapt to the fast-growing forces. Moreover, we also elucidate how the viscoelastic properties of the substrate regulate these nonlinear responses and alter cellular behaviours.

scholarly journals Dissipation of contractile forces: the missing piece in cell mechanics

2017 ◽  
Vol 28 (14) ◽  
pp. 1825-1832 ◽  
Author(s):  
Laetitia Kurzawa ◽  
Benoit Vianay ◽  
Fabrice Senger ◽  
Timothée Vignaud ◽  
Laurent Blanchoin ◽  
...  
Keyword(s):  
Cell Mechanics ◽  
Force Production ◽  
Traction Force ◽  
Structural Rearrangements ◽  
Force Transmission ◽  
Traction Forces ◽  
Cell Traction Forces ◽  
Cell Traction ◽  
Contractile Forces ◽  
Fiber Contraction

Mechanical forces are key regulators of cell and tissue physiology. The basic molecular mechanism of fiber contraction by the sliding of actin filament upon myosin leading to conformational change has been known for decades. The regulation of force generation at the level of the cell, however, is still far from elucidated. Indeed, the magnitude of cell traction forces on the underlying extracellular matrix in culture is almost impossible to predict or experimentally control. The considerable variability in measurements of cell-traction forces indicates that they may not be the optimal readout to properly characterize cell contractile state and that a significant part of the contractile energy is not transferred to cell anchorage but instead is involved in actin network dynamics. Here we discuss the experimental, numerical, and biological parameters that may be responsible for the variability in traction force production. We argue that limiting these sources of variability and investigating the dissipation of mechanical work that occurs with structural rearrangements and the disengagement of force transmission is key for further understanding of cell mechanics.

Tissue engineering science: Consequences of cell traction force

1992 ◽  
Vol 10 (3) ◽  
pp. 225-250 ◽  
Author(s):  
Robert T. Tranquillo ◽  
Mohammed A. Durrani ◽  
Alice G. Moon
Keyword(s):  
Tissue Engineering ◽  
Traction Force ◽  
Engineering Science ◽  
Cell Traction

scholarly journals Remanent cell traction force in renal vascular smooth muscle cells induced by integrin-mediated mechanotransduction

2013 ◽  
Vol 304 (4) ◽  
pp. C382-C391 ◽  
Author(s):  
Lavanya Balasubramanian ◽  
Chun-Min Lo ◽  
James S. K. Sham ◽  
Kay-Pong Yip
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Resistance ◽  
Vascular Smooth Muscle Cells ◽  
Traction Force ◽  
Muscle Cells ◽  
Myogenic Response ◽  
Cell Traction ◽  
Renal Vascular

It was previously demonstrated in isolated renal vascular smooth muscle cells (VSMCs) that integrin-mediated mechanotransduction triggers intracellular Ca2+ mobilization, which is the hallmark of myogenic response in VSMCs. To test directly whether integrin-mediated mechanotransduction results in the myogenic response-like behavior in renal VSMCs, cell traction force microscopy was used to monitor cell traction force when the cells were pulled with fibronectin-coated or low density lipoprotein (LDL)-coated paramagnetic beads. LDL-coated beads were used as a control for nonintegrin-mediated mechanotransduction. Pulling with LDL-coated beads increased the cell traction force by 61 ± 12% (9 cells), which returned to the prepull level after the pulling process was terminated. Pulling with noncoated beads had a minimal increase in the cell traction force (12 ± 9%, 8 cells). Pulling with fibronectin-coated beads increased the cell traction force by 56 ± 20% (7 cells). However, the cell traction force was still elevated by 23 ± 14% after the pulling process was terminated. This behavior is analogous to the changes of vascular resistance in pressure-induced myogenic response, in which vascular resistance remains elevated after myogenic constriction. Fibronectin is a native ligand for α5β1-integrins in VSMCs. Similar remanent cell traction force was found when cells were pulled with beads coated with β1-integrin antibody (Ha2/5). Activation of β1-integrin with soluble antibody also triggered variations of cell traction force and Ca2+ mobilization, which were abolished by the Src inhibitor. In conclusion, mechanical force transduced by α5β1-integrins triggered a myogenic response-like behavior in isolated renal VSMCs.

Abstract 1098: Mechano-molecular imaging of the role of COX-2 in cell traction force.

2013 ◽  
Author(s):  
A Rum Yoon ◽  
Ioannis Stasinopoulos ◽  
Steven An ◽  
Zaver M. Bhujwalla
Keyword(s):  
Molecular Imaging ◽  
Traction Force ◽  
Cell Traction ◽  
Cox 2

Alpha-smooth muscle actin expression enhances cell traction force

2007 ◽  
Vol 64 (4) ◽  
pp. 248-257 ◽  
Author(s):  
Jianxin Chen ◽  
Hongxia Li ◽  
Nirmala SundarRaj ◽  
James H.-C. Wang
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Traction Force ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Cell Traction ◽  
Actin Expression

Developing a multi-functional sensor for cell traction force, matrix remodeling and biomechanical assays in self-assembled 3D tissues in vitro

2021 ◽  
Author(s):  
Bashar Emon ◽  
M Saddam H Joy ◽  
M Taher A Saif
Keyword(s):  
Traction Force ◽  
Patient Specific ◽  
Matrix Remodeling ◽  
Tissue Stiffness ◽  
Cell Traction ◽  
Primary Fibroblasts ◽  
Multiple Cell ◽  
Cell Matrix Interactions ◽  
Cell Force

Abstract Cell-matrix interactions, mediated by cellular force and matrix remodeling, result in a dynamic reciprocity that drives numerous biological processes and disease progression. Currently, there is no available method for direct quantification cell traction force and matrix remodeling in 3D matrices as a function of time. To address this long-standing need, we recently developed a high-resolution microfabricated sensor1 that measures cell force, tissue-stiffness and can apply mechanical stimulation to the tissue. Here the tissue self-assembles and self-integrates with the sensor. With primary fibroblasts, cancer cells and neurons, we demonstrated the feasibility of the sensor by measuring single/multiple cell force with a resolution of 1 nN, and tissue stiffness1 due to matrix remodeling by the cells. The sensor can be translated into a high-throughput system for clinical assays such as patient-specific drug and phenotypic screening. In this paper, we present the detailed protocol for manufacturing the sensors, preparing experimental setup, developing assays with different tissues, and for imaging and analyzing the data.

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