| Description |
The ineffectiveness of wound healing devices to address chronic or long-lasting wounds is due to our lack of understanding of the ideal three-dimensional (3D) environment for wound healing. This insufficient knowledge is due to limitations in our ability to experimentally isolate complex cellular interactions between the mechanical and microstructural properties of the 3D ECM that regulate wound healing. This study aims to develop a lattice-point-based computational model to understand how the ECM's mechanical and microstructural properties and cell properties interact to modulate cell migration and proliferation. The model represents various different lattice point-based ECM based on user-input microstructural, mechanical, and cell properties. Notably, the force feedback interactions between the cell and the ECM regulates the model's mechanism of cell migration. The interactions were modeled using the Molecular Clutch Model. We found that increases in ECM porosity and decreases in ECM pore size (pore diameter) led to an overall increase in average cell migratory rates (cell speeds). These trends are consistent with other investigators and demonstrate the model's ability to simulate some microstructural interactions. Furthermore, we found a biphasic trend (an increasing then decreasing phase) modeled by the Molecular Clutch Model and observed with the interplay between the ECM's mechanical property of stiffness and cell migration rates. This trend was maintained even when changing various other ECM properties, potentially demonstrating explanations for conflicting trends from other investigators. Understanding these ECM microstructural and mechanical trends on cell migration may inform a greater understanding of 3D cell behavior and improve chronic wound care. |
