Cell locomotion is a result of a series of synchronized chemo-mechanical processes. Crawling-type cell locomotion consists of three steps: protrusion, translocation, and retraction. Previous works have shown that both protrusion and retraction can produce cell movement. For the latter, a cell derives its propulsive force from retraction induced protrusion mechanism, which was experimentally verified by Chen (1979, “Induction of Spreading During Fibroblast Movement,” J. Cell Biol., 81, pp. 684–691). In this paper, using finite element method, we take a computational biomimetic approach to study cell crawling assisted by contractile stress induced de-adhesion at the rear of the focal adhesion zone (FAZ). We assume the formation of the FAZ is driven by receptor-ligand bonds and nonspecific interactions. The contractile stress is generated due to the molecular activation of the intracellular actin-myosin machinery. The exerted contractile stress and its time dependency are modeled in a phenomenological manner as a two-spring mechanosensor proposed by Schwarz (2006, “Focal Adhesions as Mechanosensors: The Two-Spring Model,” BioSystems, 83(2–3), pp. 225–232). Through coupling the kinetics of receptor-ligand bonds with contractile stress, de-adhesion can be achieved when the stall value of the contractile stress is larger than a critical one. De-adhesion at the rear end of the FAZ causes a redistribution of elastic energy and induces cell locomotion. Parametric studies were conducted to investigate the connection between the cell locomotion speed and stall stress, and receptor-ligand kinetics. Finally, we provide a scaling relationship that can be used to estimate the cell locomotion speed.
Cell locomotion and focal adhesions are regulated by substrate flexibility
