Determination of cellular strains by combined atomic force microscopy and finite element modeling

Many organs adapt to their mechanical environment as a result of physiological change or disease. Cells are both the detectors and effectors of this process. Though many studies have been performed in vitro to investigate the mechanisms of detection and adaptation to mechanical strains, the cellular strains remain unknown and results from different stimulation techniques cannot be compared. By combining experimental determination of cell profiles and elasticities by atomic force microscopy with finite element modeling and computational fluid dynamics, we report the cellular strain distributions exerted by common whole-cell straining techniques and from micromanipulation techniques, hence enabling their comparison. Using data from our own analyses and experiments performed by others, we examine the threshold of activation for different signal transduction processes and the strain components that they may detect. We show that modulating cell elasticity, by increasing the F-actin content of the cytoskeleton, or cellular Poisson ratio are good strategies to resist fluid shear or hydrostatic pressure. We report that stray fluid flow in some substrate-stretch systems elicits significant cellular strains. In conclusion, this technique shows promise in furthering our understanding of the interplay among mechanical forces, strain detection, gene expression, and cellular adaptation in physiology and disease

La relation d’amitié et ses représentations chez des écoliers de quatre à cinq ans

À l’âge de quatre et cinq ans, les amitiés se développent quasi-exclusivement en milieu scolaire en France. En effet, l’école maternelle est l’une des premières instances de socialisation permettant aux jeunes enfants d’interagir entre pairs. Ce processus de socialisation se fait de manière différenciée selon le sexe des enfants. L’observation des relations amicales à l’école maternelle révèle ainsi l’existence de « rites » amicaux proprement scolaires, ainsi que la prégnance des stéréotypes de genre dans la construction des amitiés à l’âge préscolaire

Stress fibres and the cortex work in tandem

Stress fibres form a fully integrated meshwork with the submembranous contractile actin cortex that generates and propagates traction forces across the entire cell

Multiplicateur de Lagrange, Condensation Statique et Conditions Unilatérales

National audienceSee http://hal.archives-ouvertes.fr/docs/00/59/27/06/ANNEX/r_4V1GJ1H7.pd

Tensile Forces and Mechanotransduction at Cell-Cell Junctions

Cell-cell junctions are specializations of the plasma membrane responsible for physically integrating cells into tissues. We are now beginning to appreciate the diverse impacts that mechanical forces exert upon the integrity and function of these junctions. Currently, this is best understood for cadherin-based adherens junctions in epithelia and endothelia, where cell-cell adhesion couples the contractile cytoskeletons of cells together to generate tissue-scale tension. Junctional tension participates in morphogenesis and tissue homeostasis. Changes in tension can also be detected by mechanotransduction pathways that allow cells to communicate with each other. In this review, we discuss progress in characterising the forces present at junctions in physiological conditions; the cellular mechanisms that generate intrinsic tension and detect changes in tension; and, finally, we consider how tissue integrity is maintained in the face of junctional stresses

Stem cell differentiation increases membrane-actin adhesion regulating cell blebability, migration and mechanics

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/K. S. is funded by an EPSRC PhD studentship. S.T. is funded by an EU Marie Curie Intra European Fellowship (GENOMICDIFF)

A question of time: tissue adaptation to mechanical forces.

While much attention has been focused on the force-generating mechanisms responsible for shaping developing embryos, less is known about the ways in which cells in animal tissues respond to mechanical stimuli. Forces will arise within a tissue as the result of processes such as local cell death, growth and division, but they can also be an indirect consequence of morphogenetic movements in neighbouring tissues or be imposed from the outside, for example, by gravity. If not dealt with, the accumulation of stress and the resulting tissue deformation can pose a threat to tissue integrity and structure. Here we follow the time-course of events by which cells and tissues return to their preferred state following a mechanical perturbation. In doing so, we discuss the spectrum of biological and physical mechanisms known to underlie mechanical homeostasis in animal tissues

Mechanics of the cellular actin cortex: from signalling to shape change

The actin cortex is a thin layer of actin, myosin, and actin binding proteins that underlies the membrane of most animal cells. It is highly dynamic and can undergo remodelling on time-scales of tens of seconds thanks to protein turnover and myosin-mediated contractions. The cortex enables cells to resist external mechanical stresses, controls cell shape, and allows cells to exert forces on their neighbours. Thus, its mechanical properties are key to its physiological function. Here, we give an overview of how cortex composition, structure, and dynamics control cortex mechanics and cell shape. We use mitosis as an example to illustrate how global and local regulation of cortex mechanics give rise to a complex series of cell shape changes.Comment: Revie

Poroelastic osmoregulation of living cell volume

Cells maintain their volume through fine intracellular osmolarity regulation. Osmotic challenges drive fluid into or out of cells causing swelling or shrinkage, respectively. The dynamics of cell volume changes depending on the rheology of the cellular constituents and on how fast the fluid permeates through the membrane and cytoplasm. We investigated whether and how poroelasticity can describe volume dynamics in response to osmotic shocks. We exposed cells to osmotic perturbations and used defocusing epifluorescence microscopy on membrane-attached fluorescent nanospheres to track volume dynamics with high spatiotemporal resolution. We found that a poroelastic model that considers both geometrical and pressurization rates captures fluid-cytoskeleton interactions, which are rate-limiting factors in controlling volume changes at short timescales. Linking cellular responses to osmotic shocks and cell mechanics through poroelasticity can predict the cell state in health, disease, or in response to novel therapeutics.Peer ReviewedPostprint (published version