Collective migration under hydrodynamic interactions -- a computational approach

TL;DR

This paper presents a computational model of substrate-based cell motility incorporating hydrodynamic interactions, predicting spontaneous collective migration driven by cell collisions and actin filament reorientation, with effects varying by Reynolds number.

Contribution

It introduces a novel computational model that combines cell motility mechanisms with hydrodynamic interactions to explain collective migration phenomena.

Findings

Hydrodynamic interactions influence collective cell migration.

Cell collisions lead to vortex annihilation and cell reorientation.

Effect of hydrodynamics diminishes at higher Reynolds numbers.

Abstract

Substrate-based cell motility is essential for fundamental biological processes, such as tissue growth, wound healing and immune response. Even if a comprehensive understanding of this motility mode remains elusive, progress has been achieved in its modeling using a whole cell physical model. The model takes into account the main mechanisms of cell motility - actin polymerization, substrate mediated adhesion and actin-myosin dynamics and combines it with steric cell-cell and hydrodynamic interactions. The model predicts the onset of collective cell migration, which emerges spontaneously as a result of inelastic collisions of neighboring cells. Each cell here modeled as an active polar gel, is accomplished with two vortices if it moves. Open collision of two cells the two vortices which come close to each other annihilate. This leads to a rotation of the cells and together with the deformation and the reorientation of the actin filaments in each cell induces alignment of these cells and leads to persistent translational collective migration. The effect for low Reynolds numbers is as strong as in the non-hydrodynamic model, but it decreases with increasing Reynolds number.