Image-based finite element modeling of alveolar epithelial cell injury during airway reopening
Image-based finite element modeling of alveolar epithelial cell injury during airway reopening
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DOI：
10.1152/japplphysiol.90688.2008
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发表时间：
2009-01-01
影响因子：
3.3
通讯作者：
Ghadiali, S. N.
中科院分区：
文献类型：
--
作者：
Dailey, H. L.;Ricles, L. M.;Ghadiali, S. N.
戴利 HL、里克斯 LM、亚尔辛 HC、加迪亚利 SN。气道重新开放期间肺泡上皮细胞损伤的基于图像的有限元建模。 J Appl Physiol 106: 221-232, 2009。首次发表于 2008 年 11 月 13 日； doi:10.1152/japplphyol.90688.2008.-急性呼吸窘迫综合征 (ARDS) 的特点是小肺气道积液。这些充满液体的气道的重新开放涉及空气-液体界面的传播，该界面对气道壁内衬的上皮细胞（EpC）施加有害的流体动力应力。先前的实验研究表明，这些流体动力应力可能导致质膜破裂（即细胞坏死），并假设细胞形态在细胞死亡中发挥作用。然而，直接实验测量细胞内的应力和应变是很困难的，并且关于气道重新打开期间上皮的机械响应（即变形）的可用数据有限。本研究的目的是使用气道重新开放期间基于图像的细胞变形有限元模型来研究细胞形态和力学如何影响细胞损伤/坏死的风险。亚汇合和汇合单层中 EpC 的共焦显微镜图像用于生成形态精确的三维有限元模型。细胞上的流体动力应力是根据充满流体的平行板流道中气泡传播的边界元解计算的。结果表明，对于相同的细胞机械性能和流体动力负载条件，亚汇合细胞比汇合细胞产生更高的膜应变。还发现应变幅度随着细胞和膜/皮层区域硬度的增加而减小，但对细胞内部硬度的变化最敏感。这些模型可能有助于确定通过改变 EpC 的特定生物力学特性来减轻气道重新开放期间细胞损伤的药物治疗。
Dailey HL, Ricles LM, Yalcin HC, Ghadiali SN. Image-based finite element modeling of alveolar epithelial cell injury during airway reopening. J Appl Physiol 106: 221-232, 2009. First published November 13, 2008; doi:10.1152/japplphysiol.90688.2008.-The acute respiratory distress syndrome (ARDS) is characterized by fluid accumulation in small pulmonary airways. The reopening of these fluid-filled airways involves the propagation of an air-liquid interface that exerts injurious hydrodynamic stresses on the epithelial cells (EpC) lining the airway walls. Previous experimental studies have demonstrated that these hydrodynamic stresses may cause rupture of the plasma membrane (i. e., cell necrosis) and have postulated that cell morphology plays a role in cell death. However, direct experimental measurement of stress and strain within the cell is intractable, and limited data are available on the mechanical response (i. e., deformation) of the epithelium during airway reopening. The goal of this study is to use image-based finite element models of cell deformation during airway reopening to investigate how cell morphology and mechanics influence the risk of cell injury/necrosis. Confocal microscopy images of EpC in subconfluent and confluent monolayers were used to generate morphologically accurate three-dimensional finite element models. Hydrodynamic stresses on the cells were calculated from boundary element solutions of bubble propagation in a fluid-filled parallel-plate flow channel. Results indicate that for equivalent cell mechanical properties and hydrodynamic load conditions, subconfluent cells develop higher membrane strains than confluent cells. Strain magnitudes were also found to decrease with increasing stiffness of the cell and membrane/cortex region but were most sensitive to changes in the cell's interior stiffness. These models may be useful in identifying pharmacological treatments that mitigate cell injury during airway reopening by altering specific biomechanical properties of the EpC.