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Comunicacions a congressos (Biomedicina)

Permanent URI for this collectionhttps://hdl.handle.net/2445/66971

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    Active wetting of epithelial tissues.
    (American Society for Cell Biology, 2017-12-01) Pérez González, Carlos; Alert Zenón, Ricard; Blanch Mercader, Carles; Gómez González, Manuel; Kolodziej, Tomasz; Bazellières, Elsa; Casademunt i Viader, Jaume; Trepat Guixer, Xavier
    Development, regeneration and cancer involve changes in cell mechanical properties that lead to drastic transitions in tissue geometry and dimensionality. Given the fluid nature of living tissues, these transitions have been experimentally studied and theoretically modelled in terms of the physics of wetting phenomena, which describes how a fluid droplet spreads on a solid surface. However, physical forces, the effective determinants of tissue spreading, have never been measured in the context of tissue wetting. Here we perform a systematic study of tissue mechanics during epithelial wetting/dewetting. We induce a progressive expression of E‐cadherin in a confined monolayer of MDA‐MB‐231 cells and, simultaneously, we measure tissue forces using Traction Force Microscopy and Monolayer Stress Microscopy. The gradual formation of intercellular junctions produces a continuous increase in tissue contractility (pMLC), triggering a two‐fold increase in tissue forces that ends up in a spontaneous wetting‐dewetting transition. To understand how this transition arises from tissue active properties, we develop a wetting model based on active gels theory. Combining theory and experiments, we find that wetting‐dewetting transition results from a competition between contractility and traction forces, which introduces a new length scale, defining a critical size for tissue wetting. Strikingly, this implies that the critical tissue contractility driving the transition is dependent on tissue size, a phenomenon that has no counterpart in passive wetting/dewetting physics. Furthermore, we find that the critical tractions, which depend linearly on substrate ligand density, are the mechanical threshold for tissue spreading. Finally, we show that long‐wavelength morphological instabilities in our fluid interface, together with active fluctuations, explain tissue shape dynamics during dewetting. We conclude that tissue spreading can be understood as an active wetting transition of a viscous polar fluid.
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    Optimal collective durotaxis through E-cadherin adhesions
    (American Society for Cell Biology, 2023-02-01) Fuente, Jesús M. de la; Sunyer, Raimon; Pallarès, Macià Esteve; Pi Jaumà, Irina; Fortunato, Isabela Corina Santos; Grazu, Valeria; Gómez González, Manuel; Roca-Cusachs Soulere, Pere; Alert Zenón, Ricard; Casademunt i Viader, Jaume; Trepat Guixer, Xavier
    The directed migration of cellular clusters enables morphogenesis, wound healing, and collective cancer invasion. Gradients of substrate stiffness are known to direct the migration of cellular clusters in a process called collective durotaxis, but underlying mechanisms remain unclear. Durotaxis has been mainly studied when mediated by focal adhesions at the extracellular matrix (ECM) interface. However, in ECM-depleted environments cells migrate through the cell-cell adhesion protein E-cadherin. Here we show that when cell adhesion is mediated by E-Cadherin, clusters of cancer cells dewet on soft substrates and wet on stiff ones. At intermediate stiffness, clusters on uniform-stiffness substrates become maximally motile, and clusters on stiffness gradients exhibit optimal durotaxis. Durotactic velocity increases with cluster size, stiffness gradient, and actomyosin activity. We first demonstrate this new migratory mode on substrates coated with E-cadherin and then establish its generality on substrates coated with extracellular matrix. We develop a physical model of three-dimensional active wetting that explains this mode of collective durotaxis in terms of a balance between in-plane active traction and tissue contractility, and out-of-plane surface tension. Finally, we show that the distribution of cluster displacements has a heavy tail, with infrequent but large cellular hops that contribute to durotactic migration. Our study demonstrates a new physical mechanism of collective durotaxis, through both cell-cell and cell-substrate adhesion ligands, based on the wetting properties of active droplets.
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    Preferències dels estudiants en relació al tema d’estudi del TFG de Farmàcia (UB)
    (Universitat de Barcelona, 2015-02) Aróztegui Trenchs, Montserrat; Bernal Serrano, Antonio; Bonet Clols, Francesc; Bosque Pueyo, Ramón; Cambras Riu, Trinitat; Canudas Teixidó, Anna-Maria; Domínguez García, Àngela; Engel Rocamora, Pablo; Escribano Ferrer, Elvira; Fernández Lastra, Cecilia; Folch Sánchez, Montserrat; López Sabater, María del Carmen; March Pujol, Marian; Marqués Villavecchia, Ana M.; Marrero González, Pedro F.; Miquel Colomé, Jordi; Muñoz Juncosa, Montserrat; Palazón Barandela, Javier; Piqué Benages, Maria Esther; Puignou i Garcia, Lluís; Pujol Dilmé, M. Dolors; Simon Pallisé, Joan; Tebar Ramon, Francesc; Ticó Grau, Josep R.; Escubedo Rafa, Elena; Zulaica Gallego, Ester
    El TFG del grau de farmàcia UB es porta a terme en el marc d’un àmbit docent principal i integra coneixements de com a mínim, dos àmbits docents addicionals atès la seva funció integradora. En el moment de definir les directrius i organització de l’assignatura, es van establir a la Facultat de Farmàcia 27 àmbits docents. Tanmateix, les característiques del TFG quan a tipus de projectes o estudis es van establir inicialment en base a tres opcions...