Cooperation of dual modes of cell motility promotes epithelial stress relaxation to accelerate wound healing

Abstract

Collective cell migration in cohesive units is vital for tissue morphogenesis, wound repair, and immune response. While the fundamental driving forces for collective cell motion stem from contractile and protrusive activities of individual cells, it remains unknown how their balance is optimized to maintain tissue cohesiveness and the fluidity for motion. Here we present a cell-based computational model for collective cell migration during wound healing that incorporates mechanochemical coupling of cell motion and adhesion kinetics with stochastic transformation of active motility forces. We show that a balance of protrusive motility and actomyosin contractility is optimized for accelerating the rate of wound repair, which is robust to variations in cell and substrate mechanical properties. This balance underlies rapid collective cell motion during wound healing, resulting from a tradeoff between tension mediated collective cell guidance and active stress relaxation in the tissue.

References in corpus (9)

• A density-independent glass transition in biological tissues
• Motility-driven glass and jamming transitions in biological tissues
• Physics of adherent cells
• Cadherin-Based Intercellular Adhesions Organize Epithelial Cell-Matrix Traction Forces
• Scaling of Traction Forces with Size of Cohesive Cell Colonies
• Propagating stress waves during epithelial expansion
• Border forces and friction control epithelial closure dynamics
• Molecular Model of the Contractile Ring
• Epithelial Wound Healing Coordinates Distinct Actin Network Architectures to Conserve Mechanical Work and Balance Power

Cited by in corpus (9)

• Physical Models of Collective Cell Migration
• Multicellular rosettes drive fluid-solid transition in epithelial tissues
• Mechanical heterogeneity in tissues promotes rigidity and controls cellular invasion
• Modeling cell migration regulated by cell-ECM micromechanical coupling
• Learning to Control Active Matter
• Controlled neighbor exchanges drive glassy behavior, intermittency and cell streaming in epithelial tissues
• Gradients in solid surface tension drive Marangoni-like motions in cell aggregates
• Modeling Multi-Cellular Dynamics Regulated by ECM-Mediated Mechanical Communication via Active Particles with Polarized Effective Attraction
• Mechanical Plasticity of Cell Membranes Enhances Epithelial Wound Closure