AI 中文总结
研究部分上皮-间质转化细胞单层生长驱动伤口闭合中流体和弹性流动，开发流化生长-弹性框架，将应变率分解量化各贡献，应用于小鼠胚胎心外膜细胞间隙，揭示组织流动性和弹性对闭合运动学的关键作用。
AI 中文摘要
大规模圆形间隙闭合发生在细胞生长和增殖变得重要的时间尺度上。生长是闭合过程的主要驱动力，而细胞伸长和插入等细胞动力学反映了对组织变形的弹性和流体贡献。我们开发了一种新型的流化生长-弹性框架，作为具有生长的麦克斯韦流体的非线性类似物。该框架将实验可观测的应变率分解为生长、弹性和流体应变率的加和，从而能够从组织运动学中分别量化这些贡献，并表征组织弹性和流动性（粘度的倒数）的作用。我们将该模型应用于小鼠胚胎心外膜细胞（MEC1）汇合单层中的大圆形间隙（直径约1.7毫米），在两种条件下，即未处理和用TGF-β处理。我们表明，组织流动性和与纤维增强相关的弹性特性对于再现闭合运动学都至关重要。具体而言，我们预测处理后的条件具有较低的流动性，与未处理条件相比，流体变形率较低，弹性变形率较高，这与实验观察结果一致。
英文摘要
Large-scale circular gap closure occurs over a time scale on which cell growth and proliferation become important. Growth is the main driver of the closing process, while cell dynamics such as elongation and intercalation reflect elastic and fluidic contributions to tissue deformation. We develop a novel fluidized growth-elasticity framework as a nonlinear analogue of a Maxwell fluid with growth. The framework decomposes the experimentally observable strain rate into the additive sum of the growth, elastic, and fluidic strain rates, thus enabling the separate quantification of these contributions from tissue kinematics and allowing the roles of tissue elasticity and fluidity (the inverse of viscosity) to be characterized. We apply the model to large circular gaps ($\sim$1.7 mm in diameter) in confluent monolayers of mouse embryonic epicardial cells (MEC1) under two conditions, without and with TGF-$β$ treatment. We show that both tissue fluidity and the elastic properties associated with fiber reinforcement are critical for reproducing the closure kinematics. Specifically, we predict that the treated condition has lower fluidity, associated with a lower fluidic deformation rate and a higher elastic deformation rate than the untreated condition, in agreement with the experimental observations.
Comments36 pages, 14 figues
