A multi-modular tensegrity model of an actin stress fiber

Luo, Yaozhi; Xu, Xiang; Lele, Tanmay P.; Kumar, Sanjay; Ingber, Donald E.

doi:10.1016/j.jbiomech.2008.05.026

Cited by 89 publications

(66 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Such theory can be extended to collagenous networks as shown in Fig. 6, where a simplified tensegrity model inspired from Luo et al (2008) [35] is introduced to represent arterial adventitia with rigid collagen fibers and compliant links between the collagen fibers [13]. Such a model may explain the results observed in the present study: under inflation loading at a constant axial stretch, fiber rotation is impossible, as it would imply a transverse strain, the fibers being rigid.…”

Section: Stack Of Imagesmentioning

confidence: 90%

Kinematics of collagen fibers in carotid arteries under tension-inflation loading

Krasny

Magoariec

Morin

et al. 2018

Journal of the Mechanical Behavior of Biomedical Materials

View full text Add to dashboard Cite

Biomechanics of the extracellular matrix in arteries determines their macroscopic mechanical behavior. In particular, the distribution of collagen fibers and bundles plays a significant role. Experimental data showed that in most arterial walls there are preferred fiber directions. However, the realignment of collagen fibers during tissue deformation is still controversial: whilst authors claim that fibers should undergo affine deformations, others showed the contrary. In order to have an insight about this important question of affine deformations at the microscopic scale, we measured the realignment of collagen fibers in the adventitia layer of carotid arteries using multiphoton microscopy combined with an unprecedented Fourier based method. We compared the realignment for two types of macroscopic loading applied on arterial segments: axial tension under constant pressure (scenario 1) and inflation under constant axial length (scenario 2). Results showed that, although the tissue underwent macroscopic stretches beyond 1.5 in the circumferential direction, fiber directions remained unchanged during scenario 2 loading. Conversely, fibers strongly realigned along the axis direction for scenario 1 loading. In both cases, the motion of collagen fibers did not satisfy affine deformations, with a significant difference between both cases: affine predictions strongly under-estimated fiber reorientations in uniaxial tension and over-estimated fiber reorientations during inflation at constant length. Finally, we explained this specific kinematics of collagen fibers by the complex tension-compression interactions between very stiff collagen fibers and compliant surrounding proteins. A tensegrity representation of the extracellular matrix in the adventitia taking into account these interactions was proposed to model the motion of collagen fibers during tissue deformation.

show abstract

Section: Stack Of Imagesmentioning

confidence: 90%

Kinematics of collagen fibers in carotid arteries under tension-inflation loading

Krasny

Magoariec

Morin

et al. 2018

Journal of the Mechanical Behavior of Biomedical Materials

View full text Add to dashboard Cite

show abstract

“…The observed effect of cytoD on myosin (Fig.5C,C') seems to imply an indirect effect of cytoD on the fluorescence distribution mediated by myosin related to its role as a component of the cellular stress fibers. [15] A direct effect of myosin acting as a molecular motor seems to be excluded due to the very limited effect of metabolic poisons on the fluorescence distribution (Fig.4D). …”

Section: Accepted M Manuscriptmentioning

confidence: 98%

“…The cytoplasm of mammalian cells possesses actin and myosin structures arranged as stress fibers and organized to generate contractile structures responsible for cellular tension [15,18,19]. These fibers in intact living cells, may shorten to generate tension as well as elongate, thereby determining also cellular elasticity.…”

mentioning

confidence: 99%

A biophysical model of intracellular distribution and perinuclear accumulation of particulate matter

Rivolta

Panariti

Collini

et al. 2011

Biophysical Chemistry

View full text Add to dashboard Cite

This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT2 AbstractWe have measured in human alveolar cells the cytoplasmic distribution of the fluorophore coumarin-6 carried by Solid Lipid Nanoparticles (SLNs) and observed a perinuclear accumulation of the fluorescence that can be described by a single exponential growth along an ideal line joining the plasma membrane to the nuclear border and by a sigmoidal relationship as a function of time. Intracellular distribution was affected by lowering the temperature from 37 to 4°C and by the disruption of cytoskeleton by cytochalasin D, but it was minimally perturbed by the inhibition of ATP dependent molecular motors. A biophysical model was developed for an accumulation of loaded particles against a diffusion gradient based on a mean field interaction energy, whose origin we ascribe to the actin structure of the cytoskeleton. The estimated value for the load diffusion coefficient was four and two orders of magnitude less than that of free coumarin-6 and of SLNs in aqueous solutions, respectively, suggesting that the load moves within the cell cytoplasm in a form still reminiscent of the nanocarrier structure.

show abstract

“…Moreover, several models of the cytoskeleton have been constructed to investigate the hypothesis that this interconnected filamentous structure can act as a mechano-signal transmitter [44][45][46][47][48][49][50][51][52][53][54][55][56]. Shafrir & [46] proposed a two-dimensional model of the cytoskeleton as a random network of rigid rods representing the actin laments and linear Hookean springs representing the actin cross-linkers.…”

Section: Introductionmentioning

confidence: 99%

Shear-induced force transmission in a multicomponent, multicell model of the endothelium

Dabagh

Jalali

Butler

et al. 2014

J. R. Soc. Interface.

View full text Add to dashboard Cite

Haemodynamic forces applied at the apical surface of vascular endothelial cells (ECs) provide the mechanical signals at intracellular organelles and through the inter-connected cellular network. The objective of this study is to quantify the intracellular and intercellular stresses in a confluent vascular EC monolayer. A novel three-dimensional, multiscale and multicomponent model of focally adhered ECs is developed to account for the role of potential mechanosensors (glycocalyx layer, actin cortical layer, nucleus, cytoskeleton, focal adhesions (FAs) and adherens junctions (ADJs)) in mechanotransmission and EC deformation. The overriding issue addressed is the stress amplification in these regions, which may play a role in subcellular localization of mechanotransmission. The model predicts that the stresses are amplified 250-600-fold over apical values at ADJs and 175-200-fold at FAs for ECs exposed to a mean shear stress of 10 dyne cm 22 . Estimates of forces per molecule in the cell attachment points to the external cellular matrix and cell-cell adhesion points are of the order of 8 pN at FAs and as high as 3 pN at ADJs, suggesting that direct force-induced mechanotransmission by single molecules is possible in both. The maximum deformation of an EC in the monolayer is calculated as 400 nm in response to a mean shear stress of 1 Pa applied over the EC surface which is in accord with measurements. The model also predicts that the magnitude of the cell-cell junction inclination angle is independent of the cytoskeleton and glycocalyx. The inclination angle of the cell-cell junction is calculated to be 6.68 in an EC monolayer, which is somewhat below the measured value (9.98) reported previously for ECs subjected to 1.6 Pa shear stress for 30 min. The present model is able, for the first time, to cross the boundaries between different length scales in order to provide a global view of potential locations of mechanotransmission.

show abstract

A multi-modular tensegrity model of an actin stress fiber

Cited by 89 publications

References 41 publications

Kinematics of collagen fibers in carotid arteries under tension-inflation loading

Kinematics of collagen fibers in carotid arteries under tension-inflation loading

A biophysical model of intracellular distribution and perinuclear accumulation of particulate matter

Shear-induced force transmission in a multicomponent, multicell model of the endothelium

Contact Info

Product

Resources

About