Mechanics of a Fiber Network Within a Non-Fibrillar Matrix: Model and Comparison with Collagen-Agarose Co-gels

Lake, Spencer P.; Hadi, Mohammad F.; Lai, Victor K.; Barocas, Victor H.

doi:10.1007/s10439-012-0584-6

Cited by 64 publications

(63 citation statements)

References 65 publications

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“…The multiscale model employed was an extension of the previously presented model of collagen gel mechanics [39][40][41][42][43] applied recently to porcine aortic failure during in-plane tests [21]. It consisted of three scales: the FE domain at the millimeter (mm) scale, representative volume elements (RVEs) at the micrometer (lm) scale, and fibers with radii at the 100 nanometer (nm) scale.…”

Section: Equationmentioning

confidence: 99%

Failure of the Porcine Ascending Aorta: Multidirectional Experiments and a Unifying Microstructural Model

Witzenburg

Dhume

Shah

et al. 2017

Journal of Biomechanical Engineering

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The ascending thoracic aorta is poorly understood mechanically, especially its risk of dissection. To make better predictions of dissection risk, more information about the multidimensional failure behavior of the tissue is needed, and this information must be incorporated into an appropriate theoretical/computational model. Toward the creation of such a model, uniaxial, equibiaxial, peel, and shear lap tests were performed on healthy porcine ascending aorta samples. Uniaxial and equibiaxial tests showed anisotropy with greater stiffness and strength in the circumferential direction. Shear lap tests showed catastrophic failure at shear stresses (150-200 kPa) much lower than uniaxial tests (750-2500 kPa), consistent with the low peel tension ($60 mN/mm). A novel multiscale computational model, including both prefailure and failure mechanics of the aorta, was developed. The microstructural part of the model included contributions from a collagenreinforced elastin sheet and interlamellar connections representing fibrillin and smooth muscle. Components were represented as nonlinear fibers that failed at a critical stretch. Multiscale simulations of the different experiments were performed, and the model, appropriately specified, agreed well with all experimental data, representing a uniquely complete structure-based description of aorta mechanics. In addition, our experiments and model demonstrate the very low strength of the aorta in radial shear, suggesting an important possible mechanism for aortic dissection.

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Section: Equationmentioning

confidence: 99%

Failure of the Porcine Ascending Aorta: Multidirectional Experiments and a Unifying Microstructural Model

Witzenburg

Dhume

Shah

et al. 2017

Journal of Biomechanical Engineering

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“…proteoglycans) represented as a solid Neo-Hookean material. This framework has been successfully used to model tissues and tissue equivalents, e.g., arteries [24], collagen-agarose cogels [25,26], as well as model tissue damage [27]. A significant gap in this model, however, is the absence of cells, which are integral components in most tissues.…”

Section: Introductionmentioning

confidence: 99%

A Multiscale Approach to Modeling the Passive Mechanical Contribution of Cells in Tissues

Lai

Hadi

Tranquillo

et al. 2013

Volume 1B: Extremity; Fluid Mechanics; Gait; Growth, Remodeling, and Repair; Heart Valves; Injury Biomechanics; Mechanotransduc

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In addition to their obvious biological roles in tissue function, cells often play a significant mechanical role through a combination of passive and active behaviors. This study focused on the passive mechanical contribution of cells in tissues by improving our multiscale model via the addition of cells, which were treated as dilute spherical inclusions. The first set of simulations considered a rigid cell, with the surrounding ECM modeled as (1) linear elastic, (2) Neo-Hookean, and (3) a fiber network. Comparison with the classical composite theory for rigid inclusions showed close agreement at low cell volume fraction. The fiber network case exhibited nonlinear stress-strain behavior and Poisson's ratios larger than the elastic limit of 0.5, characteristics similar to those of biological tissues. The second set of simulations used a fiber network for both the cell (simulating cytoskeletal filaments) and matrix, and investigated the effect of varying relative stiffness between the cell and matrix, as well as the effect of a cytoplasmic pressure to enforce incompressibility of the cell. Results showed that the ECM network exerted negligible compression on the cell, even when the stiffness of fibers in the network was increased relative to the cell. Introduction of a cytoplasmic pressure significantly increased the stresses in the cell filament network, and altered how the cell changed its shape under tension. Findings from this study have implications on understanding how cells interact with their surrounding ECM, as well as in the context of mechanosensation.

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“…to have com-parable morphologies, the numerically applied stretch needs to be 30% lower than the experimentally applied stretch. The mechanically-induced reorientation of collagen fibers was the focus of several contributions, studying different collageneous tissues, such as tendon [32], collagenous constructs [10], skin [4,36], bovine pericardium [5], liver capsule [29], and carotid artery [31]. The debated question concerns the affine character of the reorientation process: do the fibers follow the strain imposed by their surrounding matrix, or are other mechanisms active in the reorientation process?…”

Section: Stack Of Imagesmentioning

confidence: 99%

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

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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.

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Mechanics of a Fiber Network Within a Non-Fibrillar Matrix: Model and Comparison with Collagen-Agarose Co-gels

Cited by 64 publications

References 65 publications

Failure of the Porcine Ascending Aorta: Multidirectional Experiments and a Unifying Microstructural Model

Failure of the Porcine Ascending Aorta: Multidirectional Experiments and a Unifying Microstructural Model

A Multiscale Approach to Modeling the Passive Mechanical Contribution of Cells in Tissues

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

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