2015/06/23 by John T. Nardini, Douglas A. Chapnick, Nardini, John T. +5
Biochemistry, Genetics and Molecular Biology · Mathematics · Medicine · #Cancer Cells and Metastasis #Cell Behavior (q-bio.CB) #Cellular Mechanics and Interactions #FOS: Biological sciences #Mathematical Biology Tumor Growth
paper · pdf · doi:10.48550/arxiv.1506.07081
openalex publication_date 2015/06/23 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/28
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.