Living soft tissues appear to promote the development and maintenance of a preferred mechanical state within a defined tolerance around a so-called set-point. This phenomenon is often referred to as mechanical homeostasis. In contradiction to the prominent role of mechanical homeostasis in various (patho)physiological processes, its underlying micromechanical mechanisms acting on the level of individual cells and fibers remain poorly understood, especially, how these mechanisms on the microscale lead to what we macroscopically call mechanical homeostasis. Here, we present a novel finite element based computational framework that is constructed bottom up, that is, it models key mechanobiological mechanisms such as actin cytoskeleton contraction and molecular clutch behavior of individual cells interacting with a reconstructed three-dimensional extracellular fiber matrix. The framework reproduces many experimental observations regarding mechanical homeostasis on short time scales (hours), in which the deposition and degradation of extracellular matrix can largely be neglected. This model can serve as a systematic tool for future in silico studies of the origin of the numerous still unexplained experimental observations about mechanical homeostasis.
翻译:活软组织似乎能促进在所谓的定点周围的固定容积范围内,发展和维护一个优选的机械状态。这种现象通常被称为机械软体保持。与机械软体保持在各种(病态)生理过程中的突出作用相反,其内在微机械机制在单细胞和纤维水平上的作用仍然不甚为人理解,特别是微尺度上的这些机械机制如何导致我们宏观所称的机械软体保持状态。在这里,我们提出了一个基于计算的新颖的有限要素框架,它由下而上地构建,即它模拟了关键机械生物机制,如细胞细胞细胞收缩和分子控制行为,与经过重建的三维外细胞纤维矩阵相互作用。这个框架复制了许多关于短时间(小时)机械软体保持的实验性观测结果,在这个短时间(小时)范围内,外细胞矩阵的沉积和退化在很大程度上可以被忽略。这个模型可以作为未来硅研究关于机械软体内大量仍在解释的实验观察结果来源的系统工具。