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