The effects of MAPK activity on cell-cell adhesion during wound healing

TL;DR

This paper presents a mathematical model to study how MAPK signaling influences cell-cell adhesion and collective migration during wound healing, showing that EGF treatment accelerates wound closure by activating MAPK pathways.

Contribution

It introduces a reaction-diffusion based model linking MAPK activity to cell adhesion and migration, providing new insights into wound healing dynamics.

Findings

MAPK activation enhances collective cell migration.

EGF treatment changes wound closure dynamics from parabolic to linear.

Model predicts increased leader cell pulling strength with MAPK activation.

Abstract

The mechanisms underlying collective migration, or the coordinated movement of a population of cells, are not well understood despite its ubiquitous nature. As a means to investigate collective migration, we consider a wound healing scenario in which a population of cells fills in the empty space left from a scratch wound. Here we present a simplified mathematical model that uses reaction-diffusion equations to model collective migration during wound healing with an emphasis on cell movement and its response to both cell signaling and cell-cell adhesion. We use the model to investigate the effect of the MAPK signaling cascade on cell-cell adhesion during wound healing after EGF treatment. Our results suggest that activation of the MAPK signaling cascade stimulates collective migration through increases in the pulling strength of leader cells. We further use the model to suggest that treating a cell population with EGF converts the time to wound closure (as function of wound area) from parabolic to linear.