Contribution of the nucleus to the mechanical properties of endothelial cells

Caille, Nathalie; Thoumine, Olivier; Tardy, Yves; Meister, Jean-Jacques

doi:10.1016/s0021-9290(01)00201-9

Cited by 494 publications

(482 citation statements)

References 33 publications

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“…Axial symmetry has been successfully used in previous computational studies to minimize computational cost (Caille et al 2002;Nguyen et al 2010;Ofek et al 2009;Haider and Guilak 2002;Rowat et al 2005). A previous 3D investigation of the role of SF contractility in the compression resistance of cells ,which used the material model employed in the current study, reported similar trends for axisymmetric and polarised cell geometries ).…”

Section: Simulations Reveal Thatsupporting

confidence: 55%

“…Axially symmetric finite element models used in the current study are based on experimental observations of spread cell morphologies (Caille et al 2002;Thoumine et al 1999). Axial symmetry has been successfully used in previous computational studies to minimize computational cost (Caille et al 2002;Nguyen et al 2010;Ofek et al 2009;Haider and Guilak 2002;Rowat et al 2005).…”

Section: Simulations Reveal Thatmentioning

confidence: 99%

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Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

Ronan

Deshpande

McMeeking

et al. 2013

Biomech Model Mechanobiol

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Publication InformationRonan, William, Deshpande, Vikram S., McMeeking, Robert M., & McGarry, J. Patrick. (2014). Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion. Biomechanics found to alter the range of substrate stiffness that cause the most significant changes in stress fibre and focal adhesion formation. Furthermore, stress fibre and focal adhesion formation evolve as a cell spreads on a substrate and leading to the formation of bands of fibres leading from the cell periphery over the nucleus. Inhibiting the formation of FAs during cell spreading is found to limit stress fibre formation. The predictions of this mutually dependent material-interface framework are strongly supported by experimental observations of cells adhered to elastic substrates and offer insight into the interdependent biomechanical processes regulating stress fibre and focal adhesion formation.

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Section: Simulations Reveal Thatsupporting

confidence: 55%

Section: Simulations Reveal Thatmentioning

confidence: 99%

Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

Ronan

Deshpande

McMeeking

et al. 2013

Biomech Model Mechanobiol

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“…pressure). The relationship between the stress tensor, σ, and strain, e, for the cell cytoplasm and nucleus was given by isotropic, linear elasticity theory according to: (5) with a Poisson's ratio, υ, of 0.33 50 and Young's moduli, E, of 775 and 1,500 Pa, for the cytoplasm and nucleus, respectively 7 (Table 1) and an applied prestress, σ 0 . The total fluid stress tensor computed from Eq.…”

Section: Finite Element Analysis Of Fluid and Solid Domainsmentioning

confidence: 99%

“…36,48,49 Although the presence or properties of the glycocalyx were not experimentally assessed in this study, we can estimate the effects of the glycocalyx on overall fluid drag on the cell using a model proposed by Weinbaum et al 55 In their calculations the glycocalyx was considered a 0.4 μm thick poroelastic Brinkman layer (for flow through porous media) mechanically coupled to the apical membrane. The Brinkman velocity, u b , was determined from: (7) where the second equation is the continuity equation. Fluid drag from the NS domain on the solid portion of the Brinkman layer was estimated by computing the forces on idealized vertical strands with N strands/unit area (Eq.…”

Section: Modeling Of the Surface Glycocalyxmentioning

confidence: 99%

Finite-Element Stress Analysis of a Multicomponent Model of Sheared and Focally-Adhered Endothelial Cells

et al. 2007

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Hemodynamic forces applied at the apical surface of vascular endothelial cells may be redistributed to and amplified at remote intracellular organelles and protein complexes where they are transduced to biochemical signals. In this study we sought to quantify the effects of cellular material inhomogeneities and discrete attachment points on intracellular stresses resulting from physiological fluid flow. Steady-state shear-and magnetic bead-induced stress, strain, and displacement distributions were determined from finite-element stress analysis of a cell-specific, multicomponent elastic continuum model developed from multimodal fluorescence images of confluent endothelial cell (EC) monolayers and their nuclei. Focal adhesion locations and areas were determined from quantitative total internal reflection fluorescence microscopy and verified using green fluorescence protein-focal adhesion kinase (GFP-FAK). The model predicts that shear stress induces small heterogeneous deformations of the endothelial cell cytoplasm on the order of <100 nm. However, strain and stress were amplified 10-100-fold over apical values in and around the high-modulus nucleus and near focal adhesions (FAs) and stress distributions depended on flow direction. The presence of a 0.4 μm glycocalyx was predicted to increase intracellular stresses by ~2-fold. The model of magnetic bead twisting rheometry also predicted heterogeneous stress, strain, and displacement fields resulting from material heterogeneities and FAs. Thus, large differences in moduli between the nucleus and cytoplasm and the juxtaposition of constrained regions (e.g. FAs) and unattached regions provide two mechanisms of stress amplification in sheared endothelial cells. Such phenomena may play a role in subcellular localization of early mechanotransduction events.

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“…When the cell is compressed sufficiently it becomes much stiffer due to the different response of the nucleus (Caille et al, 2002), and to capture this we assume that f 2 is given as follows:…”

Section: Article In Pressmentioning

confidence: 99%

How cellular movement determines the collective force generated by the Dictyostelium discoideum slug

Dallon

Othmer

2004

Journal of Theoretical Biology

106

132

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How the collective motion of cells in a biological tissue originates in the behavior of a collection of individuals, each of which responds to the chemical and mechanical signals it receives from neighbors, is still poorly understood. Here we study this question for a particular system, the slug stage of the cellular slime mold Dictyostelium discoideum (Dd). We investigate how cells in the interior of a migrating slug can effectively transmit stress to the substrate and thereby contribute to the overall motive force. Theoretical analysis suggests necessary conditions on the behavior of individual cells, and computational results shed light on experimental results concerning the total force exerted by a migrating slug. The model predicts that only cells in contact with the substrate contribute to the translational motion of the slug. Since the model is not based specifically on the mechanical properties of Dd cells, the results suggest that this behavior will be found in many developing systems. r

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Contribution of the nucleus to the mechanical properties of endothelial cells

Cited by 494 publications

References 33 publications

Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

Finite-Element Stress Analysis of a Multicomponent Model of Sheared and Focally-Adhered Endothelial Cells

How cellular movement determines the collective force generated by the Dictyostelium discoideum slug

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