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Trepat, Xavier

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Trepat

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Xavier

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Trepat, Xavier
Author's Publications: search.filters.isAuthorOfPublication.03063435-7f23-4aec-8ce4-11bb73241e0b

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    Long-lived force patterns and deformation waves at repulsive epithelial boundaries
    (Springer Science and Business Media LLC, 2017-09-11) Rodríguez-Franco, Pilar; Brugués, Agustí; Marín-Llauradó, Ariadna; Conte, Vito; Solanas, Guiomar; Batlle, Eduard; Fredberg, Jeffrey; Roca-Cusachs, Pere; Sunyer, Raimon; Trepat, Xavier
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    Propulsion and navigation within the advancing monolayer sheet
    (Springer Nature, 2013) Kim, Jae Hun; Serra-Picamal, Xavier; Tambe, Dhananjay; Zhou, Enhua; Park, Chan Young; Sadati, Monirosadat; Park, Jin-Ah; Krishnan, Ramaswamy; Gweon, Bomi; Millet, Emil; Butler, James P.; Trepat, Xavier; Fredberg, Jeffrey
    As a wound heals, or a body plan forms, or a tumour invades, observed cellular motions within the advancing cell swarm are thought to stem from yet to be observed physical stresses that act in some direct and causal mechanical fashion. Here we show that such a relationship between motion and stress is far from direct. Using monolayer stress microscopy, we probed migration velocities, cellular tractions and intercellular stresses in an epithelial cell sheet advancing towards an island on which cells cannot adhere. We found that cells located near the island exert tractions that pull systematically towards this island regardless of whether the cells approach the island, migrate tangentially along its edge, or paradoxically, recede from it. This unanticipated cell-patterning motif, which we call kenotaxis, represents the robust and systematic mechanical drive of the cellular collective to fill unfilled space.
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    Monolayer Stress Microscopy: Limitations, Artifacts, and Accuracy of Recovered Intercellular Stresses
    (Public Library of Science, 2013) Tambe, Dhananjay; Croutelle, Ugo; Trepat, Xavier; Park, Chan Young; Kim, Jae Hun; Millet, Emil; Butler, James; Fredberg, Jeffrey
    In wound healing, tissue growth, and certain cancers, the epithelial or the endothelial monolayer sheet expands. Within the expanding monolayer sheet, migration of the individual cell is strongly guided by physical forces imposed by adjacent cells. This process is called plithotaxis and was discovered using Monolayer Stress Microscopy (MSM). MSM rests upon certain simplifying assumptions, however, concerning boundary conditions, cell material properties and system dimensionality. To assess the validity of these assumptions and to quantify associated errors, here we report new analytical, numerical, and experimental investigations. For several commonly used experimental monolayer systems, the simplifying assumptions used previously lead to errors that are shown to be quite small. Out-of-plane components of displacement and traction fields can be safely neglected, and characteristic features of intercellular stresses that underlie plithotaxis remain largely unaffected. Taken together, these findings validate Monolayer Stress Microscopy within broad but well-defined limits of applicability.
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    Reinforcement versus Fluidization in Cytoskeletal Mechanoresponsiveness
    (Public Library of Science, 2009) Heintzmann, Rainer; Krishnan, Ramaswamy; Park, Chan Young; Lin, Yu-Chun; Mead, Jere; Jaspers, Richard T.; Trepat, Xavier; Lenormand, Guillaume; Tambe, Dhananjay; Smolensky, Alexander; Knoll, Andrew; Butler, James; Fredberg, Jeffrey
    Every adherent eukaryotic cell exerts appreciable traction forces upon its substrate. Moreover, every resident cell within the heart, great vessels, bladder, gut or lung routinely experiences large periodic stretches. As an acute response to such stretches the cytoskeleton can stiffen, increase traction forces and reinforce, as reported by some, or can soften and fluidize, as reported more recently by our laboratory, but in any given circumstance it remains unknown which response might prevail or why. Using a novel nanotechnology, we show here that in loading conditions expected in most physiological circumstances the localized reinforcement response fails to scale up to the level of homogeneous cell stretch; fluidization trumps reinforcement. Whereas the reinforcement response is known to be mediated by upstream mechanosensing and downstream signaling, results presented here show the fluidization response to be altogether novel: it is a direct physical effect of mechanical force acting upon a structural lattice that is soft and fragile. Cytoskeletal softness and fragility, we argue, is consistent with early evolutionary adaptations of the eukaryotic cell to material properties of a soft inert microenvironment.