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by Keyword: Fluid shear
Gonzalez-Martin, Miguel, Martinez-Ara, Guillermo, Ngo, John T, Trepat, Xavier, Roca-Cusachs, Pere, (2025). Synthetic mechanotransduction Nature Reviews Bioengineering
Cells sense mechanical forces and convert them into biochemical signals - a phenomenon called mechanotransduction, which regulates fundamental processes in health and disease. Cells can also be engineered to have exogenous, artificial mechanotransduction mechanisms; such systems implement a synthetic form of mechanotransduction, which could be applied to revert malignant phenotypes, modulate immunotherapies or to develop diagnostic tools. Here we review the status of the nascent field of synthetic mechanotransduction. First, we summarize the types of molecular mechanism known to be involved in endogenous mechanotransduction. Then, we explain how, by taking inspiration from endogenous systems, synthetic mechanotransduction systems have been developed. In its simpler form, these systems involve the expression of synthetic genes responding to natural force-sensing (mechanosensitive) proteins. In a more advanced form, they also include synthetic mechanosensitive proteins. Additionally, other systems have been developed to control force generation itself, resulting in control of tissue shape and function. Finally, we review general considerations for the design of synthetic mechanotransduction systems, and future challenges and opportunities.
JTD Keywords: Activation, Cell-adhesion, Fluid shear-stress, Force transmission, Integrin, Mechanical-stress, Membrane tension, Notch, Nuclear-envelope, Optogenetic control
Barbacena, P, Dominguez-Cejudo, M, Fonseca, CG, Gómez-González, M, Faure, LM, Zarkada, G, Pena, A, Pezzarossa, A, Ramalho, D, Giarratano, Y, Ouarné, M, Barata, D, Fortunato, IC, Misikova, LH, Mauldin, I, Carvalho, Y, Trepat, X, Roca-Cusachs, P, Eichmann, A, Bernabeu, MO, Franco, CA, (2022). Competition for endothelial cell polarity drives vascular morphogenesis in the mouse retina Developmental Cell 57, 2321-2333 
Blood-vessel formation generates unique vascular patterns in each individual. The principles governing the apparent stochasticity of this process remain to be elucidated. Using mathematical methods, we find that the transition between two fundamental vascular morphogenetic programs-sprouting angiogenesis and vascular remodeling-is established by a shift of collective front-to-rear polarity of endothelial cells in the mouse retina. We demonstrate that the competition between biochemical (VEGFA) and mechanical (blood-flow-induced shear stress) cues controls this collective polarity shift. Shear stress increases tension at focal adhesions overriding VEGFA-driven collective polarization, which relies on tension at adherens junctions. We propose that vascular morphogenetic cues compete to regulate individual cell polarity and migration through tension shifts that translates into tissue-level emergent behaviors, ultimately leading to uniquely organized vascular patterns.Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.
JTD Keywords: activation, angiogenesis, dynamics, flow, forces, image, mechanisms, vinculin, Angiogenesis, Cell polarity, Fluid shear, Mechanobiology, Morphogenesis, Shear stress
