Speaker
Description
While the biochemistry of blood coagulation is well understood, less is known about how the mechanobiology of platelets influences clot remodeling and thus initiates tissue repair. Platelets not only release biochemical components needed to rapidly form fibrin-rich thrombi but also initiate wound site contraction. Research has shown that platelets are responsible for assembling the initial fibronectin fibers, preceding the infiltration of other cells. It is now well established that cellular motility results from the polymerization of actin, the most abundant protein in eukaryotic cells, into an interconnected set of filaments. We portray this process in a continuum mechanics framework, claiming that polymerization promotes a mechanical swelling in a narrow zone around the nucleation loci, which ultimately results in cellular or bacterial motility. To investigate the mechanobiology of these processes, state-of-the-art microscopy has been combined with a novel theory, leading to advanced modeling and simulations. With respect to most published mixture theories, we abandoned the assumption of incompressibility of all constituents and extended the classical theory of Larché-Cahn chemo-transport-mechanics. The theory appears to suit well in modeling cell motility and might also work well in other mechanobiological areas of interest for our project dealii-X.
