论文标题
部分可观测时空混沌系统的无模型预测
Active wetting of epithelial tissues: modeling considerations
论文作者
论文摘要
形态发生,组织再生和癌症侵袭涉及组织形态中的过渡。这些由集体细胞迁移(CCM)引起的转变已被解释为主动润湿/润湿过渡。在模型系统上考虑了这种现象,例如在刚性底物上润湿细胞聚集体,其中包括细胞骨料运动和细胞单各向同性/各向异性散布,细胞单层围绕骨料的骨料扩散,取决于底物刚度和骨料大小。该模型系统解释了3D上皮聚集体与2D细胞单层之间的过渡,作为:(1)组织表面张力,(2)底物基质的表面张力,((3)界面界面介质张力,((4)界面张力梯度((4)由ccm和6)visconrastirs引起的近距离抗固定梯度,(5)viscoration。这些物理参数取决于细胞收缩性和细胞 - 细胞基质粘附接触的状态,以及由CCM引起的细胞系统的拉伸/压缩。尽管广泛的研究致力于研究细胞润湿,但我们仍然不了解这些物理参数之间引起细胞重排的振荡趋势的相互作用。这篇综述着重于这些物理参数在上皮润湿的背景下管理细胞重排的这些物理参数,de-wetting以及旨在重现和理解这些生物系统的建模方法。在这种情况下,我们不仅回顾了由CCM引起的细胞重排的先前发布的生物物理学模型,而且还提出了这些模型的新扩展,以指出细胞 - 矩阵界面互动张力与上皮粘弹性之间的相互作用,以及细胞扩散中的室间张力梯度的作用。
Morphogenesis, tissue regeneration and cancer invasion involve transitions in tissue morphology. These transitions, caused by collective cell migration (CCM), have been interpreted as active wetting/de-wetting transitions. This phenomenon is considered on model system such as wetting of cell aggregate on rigid substrate which includes cell aggregate movement and isotropic/anisotropic spreading of cell monolayer around the aggregate depending on the substrate rigidity and aggregate size. This model system accounts for the transition between 3D epithelial aggregate and 2D cell monolayer as a product of: (1) tissue surface tension, (2) surface tension of substrate matrix, (3) cell-matrix interfacial tension, (4) interfacial tension gradient, (5) viscoelasticity caused by CCM, and (6) viscoelasticity of substrate matrix. These physical parameters depend on the cell contractility and state of cell-cell and cell matrix adhesion contacts, as well as, the stretching/compression of cellular systems caused by CCM. Despite extensive research devoted to study cell wetting, we still do not understand interplay among these physical parameters which induces oscillatory trend of cell rearrangement. This review focuses on these physical parameters in governing the cell rearrangement in the context of epithelial aggregate wetting.de-wetting, and on the modelling approaches aimed at reproducing and understanding these biological systems. In this context, we do not only review previously-published bio-physics models for cell rearrangement caused by CCM, but also propose new extensions of those models in order to point out the interplay between cell-matrix interfacial tension and epithelial viscoelasticity and the role of the interfacial tension gradient in cell spreading.