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Impact of physiological loads of arterial wall on nucleus deformation in endothelial cells: A computational study

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216305%3A26210%2F22%3APU143255" target="_blank" >RIV/00216305:26210/22:PU143255 - isvavai.cz</a>

  • Výsledek na webu

    <a href="https://www.sciencedirect.com/science/article/pii/S0010482522000580" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0010482522000580</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.compbiomed.2022.105266" target="_blank" >10.1016/j.compbiomed.2022.105266</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Impact of physiological loads of arterial wall on nucleus deformation in endothelial cells: A computational study

  • Popis výsledku v původním jazyce

    Introduction: Computational modeling can enhance the understanding of cell mechanics. To achieve this, finite element models of endothelial cells were proposed with shapes mimicking their natural state inside the endothelium within the cardiovascular system. Implementing the recently proposed bendo-tensegrity concept, these models consider flexural (buckling) as well as tensional/compressional behavior of microtubules and also incorporate the waviness of intermediate filaments. Materials and methods: Four different models were created (flat and domed hexagons, both regular and elongated in the direction of blood flow) and loaded by biaxial deformation, blood pressure, and shear load from blood flow - natural physiological conditions of the arterial endothelium - aiming to investigate the "in situ" mechanical response of the cell. Results: The impact of individual components of loads on the nucleus deformation (more specifically on the first principal strain) potentially influencing mechanotransduction was investigated and the role of the cytoskeleton and its constituents in the mechanical response of the endothelial cell was assessed. The results show (i) the impact of pulsating blood pressure on cyclic deformations of the nucleus, which increase substantially with decreasing axial pre-stretch of the cell, (ii) the importance of relatively low shear stresses in the cell response and nucleus deformation. Conclusion: Not only the pulsatile blood pressure but also the wall shear stress may induce significant deformation of the nucleus and thus trigger remodelation processes in endothelial cells.

  • Název v anglickém jazyce

    Impact of physiological loads of arterial wall on nucleus deformation in endothelial cells: A computational study

  • Popis výsledku anglicky

    Introduction: Computational modeling can enhance the understanding of cell mechanics. To achieve this, finite element models of endothelial cells were proposed with shapes mimicking their natural state inside the endothelium within the cardiovascular system. Implementing the recently proposed bendo-tensegrity concept, these models consider flexural (buckling) as well as tensional/compressional behavior of microtubules and also incorporate the waviness of intermediate filaments. Materials and methods: Four different models were created (flat and domed hexagons, both regular and elongated in the direction of blood flow) and loaded by biaxial deformation, blood pressure, and shear load from blood flow - natural physiological conditions of the arterial endothelium - aiming to investigate the "in situ" mechanical response of the cell. Results: The impact of individual components of loads on the nucleus deformation (more specifically on the first principal strain) potentially influencing mechanotransduction was investigated and the role of the cytoskeleton and its constituents in the mechanical response of the endothelial cell was assessed. The results show (i) the impact of pulsating blood pressure on cyclic deformations of the nucleus, which increase substantially with decreasing axial pre-stretch of the cell, (ii) the importance of relatively low shear stresses in the cell response and nucleus deformation. Conclusion: Not only the pulsatile blood pressure but also the wall shear stress may induce significant deformation of the nucleus and thus trigger remodelation processes in endothelial cells.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    10602 - Biology (theoretical, mathematical, thermal, cryobiology, biological rhythm), Evolutionary biology

Návaznosti výsledku

  • Projekt

    Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

  • Návaznosti

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Ostatní

  • Rok uplatnění

    2022

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    COMPUTERS IN BIOLOGY AND MEDICINE

  • ISSN

    0010-4825

  • e-ISSN

    1879-0534

  • Svazek periodika

    143

  • Číslo periodika v rámci svazku

    143

  • Stát vydavatele periodika

    US - Spojené státy americké

  • Počet stran výsledku

    11

  • Strana od-do

    „105266-1“-„105266-11“

  • Kód UT WoS článku

    000788097600006

  • EID výsledku v databázi Scopus

    2-s2.0-85123378653