A Prestressed Cable Network Model of the Adherent Cell Cytoskeleton

Coughlin, Mark F.; Stamenović, Dimitrije

doi:10.1016/s0006-3495(03)74948-0

Cited by 89 publications

(82 citation statements)

References 39 publications

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“…Thus, as predicted by the tensegrity model, continuous transmission of tension between different cytoskeletal filament systems, and from the cytoskeleton to both the nucleus and ECM receptors, is critical for cell shape stability. Interestingly, even the submembranous cytoskeleton (the cortical actin-ankyrin-spectrin lattice) appears to require tensional prestress for its mechanical stability (Discher et al, 1998;Coughlin and Stamenovic, 2003).…”

Section: Prestress Is a Major Determinant Of Cell Mechanicsmentioning

confidence: 99%

“…they lack internal compression struts) can mimic the cell's response to generalized membrane deformation (e.g. owing to poking of a cell with an uncoated micropipette), they cannot explain many other cell mechanical behaviors, especially those that are measured through cell-surface receptors that link to the internal cytoskeleton (Coughlin and Stamenovic, 2003).…”

Section: Mathematical Formulation Of the Tensegrity Theorymentioning

confidence: 99%

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Tensegrity I. Cell structure and hierarchical systems biology

Ingber

2003

Journal of Cell Science

1,118

795

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In 1993, a Commentary in this journal described how a simple mechanical model of cell structure based on tensegrity architecture can help to explain how cell shape, movement and cytoskeletal mechanics are controlled, as well as how cells sense and respond to mechanical forces (J. Cell Sci.104, 613-627). The cellular tensegrity model can now be revisited and placed in context of new advances in our understanding of cell structure,biological networks and mechanoregulation that have been made over the past decade. Recent work provides strong evidence to support the use of tensegrity by cells, and mathematical formulations of the model predict many aspects of cell behavior. In addition, development of the tensegrity theory and its translation into mathematical terms are beginning to allow us to define the relationship between mechanics and biochemistry at the molecular level and to attack the larger problem of biological complexity. Part I of this two-part article covers the evidence for cellular tensegrity at the molecular level and describes how this building system may provide a structural basis for the hierarchical organization of living systems — from molecule to organism. Part II, which focuses on how these structural networks influence information processing networks, appears in the next issue.

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Section: Prestress Is a Major Determinant Of Cell Mechanicsmentioning

confidence: 99%

Section: Mathematical Formulation Of the Tensegrity Theorymentioning

confidence: 99%

Tensegrity I. Cell structure and hierarchical systems biology

Ingber

2003

Journal of Cell Science

1,118

795

View full text Add to dashboard Cite

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“…Experiments, however, have shown that the strain field is far from homogeneous, is widely distributed throughout the cell, and tends to be focused at regions around focal adhesions, so there are clearly additional structural features that need to be incorporated into the models. One aspect, the discrete nature of the force-transmitting filaments, is included in the theoretical analyses of tensegrity structures (17). Other factors associated, for example, with the localized attachment of the cell via focal adhesions also need to be considered in all these models.…”

Section: Force Transduction Pathways and Signalingmentioning

confidence: 99%

Cell mechanics and mechanotransduction: pathways, probes, and physiology

Huang

Kamm²,

Lee³

2004

American Journal of Physiology-Cell Physiology

484

367

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not only a complex biochemical environment but also a diverse biomechanical environment. How cells respond to variations in mechanical forces is critical in homeostasis and many diseases. The mechanisms by which mechanical forces lead to eventual biochemical and molecular responses remain undefined, and unraveling this mystery will undoubtedly provide new insight into strengthening bone, growing cartilage, improving cardiac contractility, and constructing tissues for artificial organs. In this article we review the physical bases underlying the mechanotransduction process, techniques used to apply controlled mechanical stresses on living cells and tissues to probe mechanotransduction, and some of the important lessons that we are learning from mechanical stimulation of cells with precisely controlled forces.cytoskeleton; micromanipulation; cell signaling ALL LIVING ORGANISMS face mechanical forces, from the fluid forces around a bacterium to the high forces in a human knee during stair climbing. The process of converting physical forces into biochemical signals and integrating these signals into the cellular responses is referred to as mechanotransduction. Although this review cannot cover all that has been discovered about mechanotransduction, we discuss the molecule-and cell-level structures that may participate in mechanotransduction, provide an overview of prominent techniques currently used for exerting mechanical stresses on cells, and conclude with an overview of the tissue-level response to mechanical signaling. FORCE TRANSDUCTION PATHWAYS AND SIGNALINGForce transmission pathways at the cellular and subcellular scales. Understanding the molecular basis for mechanotransduction requires knowledge of the magnitude and distribution of forces throughout the cell at the molecular scale. At present, we have sufficient information to measure molecular scale forces in only a very few cases. We can, however, analyze the mechanisms by which force is transmitted throughout the cell and use that as a basis for speculation about the molecular mechanisms of mechanotransduction. A variety of different methods have been used to mechanically stimulate a cell, and the cellular response is multifaceted and diverse. Similarly, there are likely to be a variety of sensing mechanisms and locations within the cell where forces can be transduced from a mechanical to a biochemical signal. Despite this apparent complexity, it is probable that cells stimulated in different ways are activated by similar mechanisms at the molecular level. To identify these commonalities, it is useful to consider how externally applied forces are transmitted into and throughout the cell, as well as the magnitudes and distribution of force corresponding to these different methods of stimulation.Both continuum and microstructural approaches have been used to determine force distributions. In the case of a continuum model, the details of the microstructure are ignored, and the forces transmitted via the individual microstructural elements are described in...

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“…Material properties have been estimated for cell constituents such as cytoskeletal proteins, cytoskeletal networks, lipid bilayers, and plasma membranes, as well as whole cells including alveolar and bronchial epithelial cells (113,114). In the context of a discussion on cell injury two characteristics of biomaterials deserve comment: (1 ) the distinct rheologic properties of network structures (115)(116)(117) and (2 ) the importance of active remodeling in determining cell plasticity (118)(119)(120).…”

Section: Microrheology Of Living Cellsmentioning

confidence: 99%

Cellular Stress Failure in Ventilator-injured Lungs

Vlahakis

Hubmayr

2005

Am J Respir Crit Care Med

188

120

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The clinical and experimental literature has unequivocally established that mechanical ventilation with large tidal volumes is injurious to the lung. However, uncertainty about the micromechanics of injured lungs and the numerous degrees of freedom in ventilator settings leave many unanswered questions about the biophysical determinants of lung injury. In this review we focus on experimental evidence for lung cells as injury targets and the relevance of these studies for human ventilator-associated lung injury. In vitro, the stress-induced mechanical interactions between matrix and adherent cells are important for cellular remodeling as a means for preventing compromise of cell structure and ultimately cell injury or death. In vivo, these same principles apply. Large tidal volume mechanical ventilation results in physical breaks in alveolar epithelial and endothelial plasma membrane integrity and subsequent triggering of proinflammatory signaling cascades resulting in the cytokine milieu and pathologic and physiologic findings of ventilatorassociated lung injury. Importantly, though, alveolar cells possess cellular repair and remodeling mechanisms that in addition to protecting the stressed cell provide potential molecular targets for the prevention and treatment of ventilator-associated lung injury in the future.

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A Prestressed Cable Network Model of the Adherent Cell Cytoskeleton

Cited by 89 publications

References 39 publications

Tensegrity I. Cell structure and hierarchical systems biology

Tensegrity I. Cell structure and hierarchical systems biology

Cell mechanics and mechanotransduction: pathways, probes, and physiology

Cellular Stress Failure in Ventilator-injured Lungs

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