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    Finite-Element Analysis of the Adhesion-Cytoskeleton-Nucleus Mechanotransduction Pathway During Endothelial Cell Rounding: Axisymmetric Model

    Source: Journal of Biomechanical Engineering:;2005:;volume( 127 ):;issue: 004::page 594
    Author:
    Ronald P. Jean
    ,
    Christopher S. Chen
    ,
    Alexander A. Spector
    DOI: 10.1115/1.1933997
    Publisher: The American Society of Mechanical Engineers (ASME)
    Abstract: Endothelial cells possess a mechanical network connecting adhesions on the basal surface, the cytoskeleton, and the nucleus. Transmission of force at adhesions via this pathway can deform the nucleus, ultimately resulting in an alteration of gene expression and other cellular changes (mechanotransduction). Previously, we measured cell adhesion area and apparent nuclear stretch during endothelial cell rounding. Here, we reconstruct the stress map of the nucleus from the observed strains using finite-element modeling. To simulate the disruption of adhesions, we prescribe displacement boundary conditions at the basal surface of the axisymmetric model cell. We consider different scenarios of the cytoskeletal arrangement, and represent the cytoskeleton as either discrete fibers or as an effective homogeneous layer. When the nucleus is in the initial (spread) state, cytoskeletal tension holds the nucleus in an elongated, ellipsoidal configuration. Loss of cytoskeletal tension during cell rounding is represented by reactive forces acting on the nucleus in the model. In our simulations of cell rounding, we found that, for both representations of the cytoskeleton, the loss of cytoskeletal tension contributed more to the observed nuclear deformation than passive properties. Since the simulations make no assumption about the heterogeneity of the nucleus, the stress components both within and on the surface of the nucleus were calculated. The nuclear stress map showed that the nucleus experiences stress on the order of magnitude that can be significant for the function of DNA molecules and chromatin fibers. This study of endothelial cell mechanobiology suggests the possibility that mechanotransduction could result, in part, from nuclear deformation, and may be relevant to angiogenesis, wound healing, and endothelial barrier dysfunction.
    keyword(s): Force , Deformation , Fibers , Stress , Engineering simulation , Finite element analysis , Boundary-value problems , Endothelial cells , Tension , Displacement AND Simulation ,
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      Finite-Element Analysis of the Adhesion-Cytoskeleton-Nucleus Mechanotransduction Pathway During Endothelial Cell Rounding: Axisymmetric Model

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    http://yetl.yabesh.ir/yetl1/handle/yetl/131357
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    • Journal of Biomechanical Engineering

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    contributor authorRonald P. Jean
    contributor authorChristopher S. Chen
    contributor authorAlexander A. Spector
    date accessioned2017-05-09T00:15:19Z
    date available2017-05-09T00:15:19Z
    date copyrightAugust, 2005
    date issued2005
    identifier issn0148-0731
    identifier otherJBENDY-26519#594_1.pdf
    identifier urihttp://yetl.yabesh.ir/yetl/handle/yetl/131357
    description abstractEndothelial cells possess a mechanical network connecting adhesions on the basal surface, the cytoskeleton, and the nucleus. Transmission of force at adhesions via this pathway can deform the nucleus, ultimately resulting in an alteration of gene expression and other cellular changes (mechanotransduction). Previously, we measured cell adhesion area and apparent nuclear stretch during endothelial cell rounding. Here, we reconstruct the stress map of the nucleus from the observed strains using finite-element modeling. To simulate the disruption of adhesions, we prescribe displacement boundary conditions at the basal surface of the axisymmetric model cell. We consider different scenarios of the cytoskeletal arrangement, and represent the cytoskeleton as either discrete fibers or as an effective homogeneous layer. When the nucleus is in the initial (spread) state, cytoskeletal tension holds the nucleus in an elongated, ellipsoidal configuration. Loss of cytoskeletal tension during cell rounding is represented by reactive forces acting on the nucleus in the model. In our simulations of cell rounding, we found that, for both representations of the cytoskeleton, the loss of cytoskeletal tension contributed more to the observed nuclear deformation than passive properties. Since the simulations make no assumption about the heterogeneity of the nucleus, the stress components both within and on the surface of the nucleus were calculated. The nuclear stress map showed that the nucleus experiences stress on the order of magnitude that can be significant for the function of DNA molecules and chromatin fibers. This study of endothelial cell mechanobiology suggests the possibility that mechanotransduction could result, in part, from nuclear deformation, and may be relevant to angiogenesis, wound healing, and endothelial barrier dysfunction.
    publisherThe American Society of Mechanical Engineers (ASME)
    titleFinite-Element Analysis of the Adhesion-Cytoskeleton-Nucleus Mechanotransduction Pathway During Endothelial Cell Rounding: Axisymmetric Model
    typeJournal Paper
    journal volume127
    journal issue4
    journal titleJournal of Biomechanical Engineering
    identifier doi10.1115/1.1933997
    journal fristpage594
    journal lastpage600
    identifier eissn1528-8951
    keywordsForce
    keywordsDeformation
    keywordsFibers
    keywordsStress
    keywordsEngineering simulation
    keywordsFinite element analysis
    keywordsBoundary-value problems
    keywordsEndothelial cells
    keywordsTension
    keywordsDisplacement AND Simulation
    treeJournal of Biomechanical Engineering:;2005:;volume( 127 ):;issue: 004
    contenttypeFulltext
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    DSpace software copyright © 2002-2015  DuraSpace
    نرم افزار کتابخانه دیجیتال "دی اسپیس" فارسی شده توسط یابش برای کتابخانه های ایرانی | تماس با یابش
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