A particle-based model for endothelial cell migration under flow conditions

Abstract

Endothelial cells (ECs) play a major role in the healing process following angioplasty to inhibit excessive neointima. This makes the process of EC healing after injury, in particular EC migration in a stented vessel, important for recovery of normal vessel function. In that context, we present a novel particle-based model of EC migration and validate it against in vitro experimental data. We have developed a particle-based model of EC migration under flow conditions in an in vitro vessel with obstacles. Cell movement in the model is a combination of random walks and directed movement along the local flow velocity vector. For model calibration, a set of experimental data for cell migration in a similarly shaped channel has been used. We have calibrated the model for a baseline case of a channel with no obstacles and then applied it to the case of a channel with ridges on the bottom surface, representative of stent strut geometry. We were able to closely reproduce the cell migration speed and angular distribution of their movement relative to the flow direction reported in vitro. The model also reproduces qualitative aspects of EC migration, such as entrapment of cells downstream from the flow-disturbing ridge. The model has the potential, after more extensive in vitro validation, to study the effect of variation in strut spacing and shape, through modification of the local flow, on EC migration. The results of this study support the hypothesis that EC migration is strongly affected by the direction and magnitude of local wall shear stress.

Numerical Study on Dynamics of Blood Cell Migration and Deformation in Atherosclerotic Vessels

“…The lattice model that is used in [14][15][16], known as the cellular Potts model, describes individual cells as domains on a lattice. Particle models, which are used in [17,18], treat each cell as one or two circular particles so that they can capture cell shape anisotropy. The phase-field model, originating in interface dynamics [19], describes each cell by a phase field ϕ. Jakob et al [20] described the movement of many self-organized, interacting cells by presenting a phase-field model that took into account the main mechanisms of cell motility acto-myosin dynamics, as well as substratemediated and cell-cell adhesion.…”