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Investigating cell mechanics with atomic force microscopy.

Kristina Haase, +1 more
- 06 Mar 2015 - 
- Vol. 12, Iss: 104, pp 20140970-20140970
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TLDR
This review generally describes the mechanotransductive process through discussion of well-known mechanosensors, and focuses on discussion of recent examples where AFM is used to specifically probe the elastic and inelastic responses of single cells undergoing deformation.
Abstract
Transmission of mechanical force is crucial for normal cell development and functioning. However, the process of mechanotransduction cannot be studied in isolation from cell mechanics. Thus, in order to understand how cells ‘feel’, we must first understand how they deform and recover from physical perturbations. Owing to its versatility, atomic force microscopy (AFM) has become a popular tool to study intrinsic cellular mechanical properties. Used to directly manipulate and examine whole and subcellular reactions, AFM allows for top-down and reconstitutive approaches to mechanical characterization. These studies show that the responses of cells and their components are complex, and largely depend on the magnitude and time scale of loading. In this review, we generally describe the mechanotransductive process through discussion of well-known mechanosensors. We then focus on discussion of recent examples where AFM is used to specifically probe the elastic and inelastic responses of single cells undergoing deformation. We present a brief overview of classical and current models often used to characterize observed cellular phenomena in response to force. Both simple mechanistic models and complex nonlinear models have been used to describe the observed cellular behaviours, however a unifying description of cell mechanics has not yet been resolved.

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Citations
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The stiffness of living tissues and its implications for tissue engineering

TL;DR: The stiffness of tissue components — from extracellular matrix and single cells to bulk tissue — is outlined, and how this understanding facilitates the engineering of materials with lifelike properties is discussed.
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The actin cortex at a glance.

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Understanding nanoparticle endocytosis to improve targeting strategies in nanomedicine

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Are cancer cells really softer than normal cells

TL;DR: It is argued that cancer cells can indeed be considered as softer than normal cells, and the intracellular elements that could be responsible for the softening of cancer cells are focused on.
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Effect of Actin Organization on the Stiffness of Living Breast Cancer Cells Revealed by Peak-Force Modulation Atomic Force Microscopy.

TL;DR: Results substantiate that actin stress fibers provide a dominant contribution to stiffness in healthy cells, while the elasticity of tumorigenic cells appears not predominantly determined by these structures.
References
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Journal ArticleDOI

Matrix elasticity directs stem cell lineage specification.

TL;DR: Naive mesenchymal stem cells are shown here to specify lineage and commit to phenotypes with extreme sensitivity to tissue-level elasticity, consistent with the elasticity-insensitive commitment of differentiated cell types.
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Rho, Rac, and Cdc42 GTPases regulate the assembly of multimolecular focal complexes associated with actin stress fibers, lamellipodia, and filopodia

TL;DR: It is reported here that cdc42, another member of the rho family, triggers the formation of a third type of actin-based structure found at the cell periphery, filopodia, in addition to stress fibers, and rho controls the assembly of focal adhesion complexes.
Journal ArticleDOI

The relation between load and penetration in the axisymmetric Boussinesq problem for a punch of arbitrary profile

TL;DR: In this article, a solution of the axisymmetric Boussinesq problem is derived from which are deduced simple formulae for the depth of penetration of the tip of a punch of arbitrary profile and for the total load which must be applied to the punch to achieve this penetration.
Journal ArticleDOI

Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation

TL;DR: It is demonstrated that the serine/threonine protein kinase Akt/PKB mediates the activation of eNOS, leading to increased NO production, and represents a novel Ca2+-independent regulatory mechanism for activation ofeNOS.
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