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PLoS Comput Biol. 2018 Oct 1;14(10):e1006502. doi: 10.1371/journal.pcbi.1006502. eCollection 2018 Oct.

Cooperation of dual modes of cell motility promotes epithelial stress relaxation to accelerate wound healing.

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Department of Physics and Astronomy, University College London, London, United Kingdom.
Institute for the Physics of Living Systems, University College London, London, United Kingdom.
Department of Physics, Northeastern University, Boston, Massachusetts, United States of America.
Department of Biomedical Engineering, Yale University, New Haven, Connecticut, United States of America.
Systems Biology Institute, Yale University, West Haven, Connecticut, United States of America.
Department of Physics, Yale University, New Haven, Connecticut, United States of America.


Collective cell migration in cohesive units is vital for tissue morphogenesis, wound repair, and immune response. While the fundamental driving forces for collective cell motion stem from contractile and protrusive activities of individual cells, it remains unknown how their balance is optimized to maintain tissue cohesiveness and the fluidity for motion. Here we present a cell-based computational model for collective cell migration during wound healing that incorporates mechanochemical coupling of cell motion and adhesion kinetics with stochastic transformation of active motility forces. We show that a balance of protrusive motility and actomyosin contractility is optimized for accelerating the rate of wound repair, which is robust to variations in cell and substrate mechanical properties. This balance underlies rapid collective cell motion during wound healing, resulting from a tradeoff between tension mediated collective cell guidance and active stress relaxation in the tissue.

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