首页> 外文会议>ASME Bioengineering Conference >CELL-TO-CELL VARIABILITY IN TENSILE STRAINS OCCURRING IN THE PLASMA MEMBRANE AND NUCLEAR SURFACE AREA OF COMPRESSED MYOBLASTS
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CELL-TO-CELL VARIABILITY IN TENSILE STRAINS OCCURRING IN THE PLASMA MEMBRANE AND NUCLEAR SURFACE AREA OF COMPRESSED MYOBLASTS

机译:在血浆膜和压制肌细胞的核表面区域中发生拉伸菌株的细胞 - 细胞变异性

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Confocal-microscopy-based three-dimensional (3D) cell-specific finite element (FE) modeling has recently been introduced by our group as a method to simulate the structural behavior of realistic cell geometries under external loading, while considering details of intracellular organelle [1,2]. This method provides comprehensive knowledge regarding cellular mechanics problems, for example, it is useful in the context of understanding the aetiology of deep tissue injury (DTI) - a type of a serious pressure ulcer associated with sustained cellular deformations [3-6]. In this regard, we previously postulated that sustained deformations of soft tissues near bony prominences could cause cell death by a mechanism of locally stretching cells, the consequence of which being that the permeability of the plasma membrane and nuclear surface area (NSA) in the affected cells increases. This, in turn, pathologically changes cell-matrix and intracellular transport profiles and eventually disrupts cellular homeostasis [1,7]. We hypothesize that tensile strains in the plasma membrane and NSA might differ in magnitude and pattern across externally-loaded individual cells of the same cell type, due to cell-to-cell morphological differences. Hence, in this study, we utilize confocal-based cell-specific 3D modeling to analyze tensile strain states in the plasma membrane and NSA of 3 different skeletal muscle cells (myoblasts) subjected to compression. We were specifically interested in chacterizing cell-to-cell variability in magnitudes and patterns of the localized strains.
机译:共焦显微术的基于三维(3D)细胞特异性有限元(FE)建模最近已经由我们的基团作为模拟下外部负载现实单元几何形状的结构行为的方法引入,同时考虑细胞内细胞器的细节[ 1,2]。该方法提供关于蜂窝力学问题全面的知识,例如,它是在理解深组织损伤(DTI)的病因学范围内有用的 - 溃疡具有持续蜂窝变形[3-6]相关联的类型严重压力。在这方面,我们之前假设骨骼突出附近的软组织的持续变形可能导致局部拉伸细胞的机制导致细胞死亡,其结果是受影响的血浆膜和核表面区域(NSA)的渗透性细胞增加。反过来,这是病理上变化细胞基质和细胞内传输曲线,最终破坏细胞稳态[1,7]。我们假设由于细胞对细胞形态差异,等离子体膜和NSA中的拉伸菌株可能与相同细胞类型的外部负载单个细胞的幅度和模式不同。因此,在本研究中,我们利用基于共组的细胞特异性三维建模来分析血浆膜中的拉伸应变状态,并进行3种不同的骨骼肌细胞(肌细胞)的NSA进行压缩。我们特别感兴趣地利用局部菌株的幅度和图案中的细胞对细胞变异性。

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