Cell and tissue mechanics in cell migration

Lange, Janina; Fabry, Ben

doi:10.1016/j.yexcr.2013.04.023

Cited by 172 publications

(126 citation statements)

References 44 publications

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“…During cell migration, dynamics reorganization of cytoskeleton in specific sites drive the cell to contraction and/or rotation. Hence, relatively loose cytoskeleton is beneficial for cell migration, either through reducing cell stiffness to easily pass through small holes or through quick degradation and assembly of cytoskeleton to lead cells stretch to crawl forward (Friedl et al 2011;Lange and Fabry 2013). In this study, we found that SMG markedly inhibited BMSCs migration, accompanied with the augmented F-actin cytoskeleton formation and abnormal cell stiffness.…”

Section: Discussionmentioning

confidence: 56%

Simulated microgravity inhibits the migration of mesenchymal stem cells by remodeling actin cytoskeleton and increasing cell stiffness

et al. 2016

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Exposure to microgravity during space flight affects almost all human physiological systems. Migration, proliferation, and differentiation of stem cells are crucial for tissues repair and regeneration. However, the effect of microgravity on the migration potentials of bone marrow mesenchymal stem cells (BMSCs) is unclear, which are important progenitor and supporting cells. Here, we utilized a clinostat to model simulated microgravity (SMG) and found that SMG obviously inhibited migration of rat BMSCs. We detected significant reorganization of F-actin filaments and increased Young's modulus of BMSCs after exposure to SMG. Moreover, Y-27632 (a specific inhibitor of ROCK) abrogated the inhibited migration capacity and polymerized F-actin filament of BMSCs under SMG. Interestingly, we found that transferring BMSCs to normal gravity also attenuated the polymerized F-actin filament and Young's modulus of BMSCs induced by SMG, but could not recover migration capacity of BMSCs inhibited by SMG. Taken together, we propose that SMG inhibits migration of BMSCs through remodeling F-actin and increasing cell stiffness.

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Section: Discussionmentioning

confidence: 56%

Simulated microgravity inhibits the migration of mesenchymal stem cells by remodeling actin cytoskeleton and increasing cell stiffness

et al. 2016

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“…For instance, cell migration, cell adhesion, and cell division have all been shown to depend on cell mechanics (1)(2)(3)(4)(5). Most studies have focused on the mechanical cross talk between the cell and its microenvironment at the whole-cell or the tissue level.…”

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confidence: 99%

Mapping intracellular mechanics on micropatterned substrates

Mandal

Asnacios

Goud

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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The mechanical properties of cells impact on their architecture, their migration, intracellular trafficking, and many other cellular functions and have been shown to be modified during cancer progression. We have developed an approach to map the intracellular mechanical properties of living cells by combining micropatterning and optical tweezers-based active microrheology. We optically trap micrometersized beads internalized in cells plated on crossbow-shaped adhesive micropatterns and track their displacement following a step displacement of the cell. The local intracellular complex shear modulus is measured from the relaxation of the bead position assuming that the intracellular microenvironment of the bead obeys power-law rheology. We also analyze the data with a standard viscoelastic model and compare with the power-law approach. We show that the shear modulus decreases from the cell center to the periphery and from the cell rear to the front along the polarity axis of the micropattern. We use a variety of inhibitors to quantify the spatial contribution of the cytoskeleton, intracellular membranes, and ATPdependent active forces to intracellular mechanics and apply our technique to differentiate normal and cancer cells.ell mechanics play a crucial role in many cellular functions that are critical during development or are altered during pathologies such as cancers. For instance, cell migration, cell adhesion, and cell division have all been shown to depend on cell mechanics (1-5). Most studies have focused on the mechanical cross talk between the cell and its microenvironment at the whole-cell or the tissue level. It has been shown recently that intracellular mechanics could also be used to differentiate cancer cells from normal cells (6-9). Several intracellular elements participate in the mechanical response of the cytoplasm, and most of them may be modified during cancer progression. The three types of fibers constituting the cytoskeleton, actin, microtubules, and intermediate filaments, clearly contribute to cell mechanics (10-13). The role of internal membranes, molecular crowding, or active force generators in the cytoplasm is less documented but could also be significant. During cancer development, signaling associated to the cytoskeleton as well as membrane trafficking, cell polarity, and intracellular organization are deregulated (14-16), supporting the idea that the mechanics of the interior of cancer cells could differ from that of normal cells.Passive or active microrheology techniques have been developed to measure intracellular mechanical properties, mostly based on the tracking of endogenous granules or internalized particles (17)(18)(19)(20)(21)(22). The experimental results are generally analyzed using two main classes of models, viscoelastic models with a finite number of viscous (dashpots) and elastic (springs) elements and power-law (PL) models (see refs. 23-26 for reviews). An increasing amount of experimental evidence points to weak PL rheology as a common feature of cell mechanical res...

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“…collective cell migration | avalanches | universality | vascular endothelial cadherin | collagen substrate C ollective cell movement depends on intracellular biological mechanisms as well as environmental cues due to the extracellular matrix (1)(2)(3)(4)(5), mainly composed of collagen which is organized in hierarchical structures, such as fibrils and fibers. The mechanical properties of collagen fibril networks are essential to offer little resistance and high sensitivity to small deformations, allowing easy local remodeling and strong strain stiffening needed to ensure cell and tissue integrity (6).…”

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confidence: 99%

Bursts of activity in collective cell migration

Chepizhko

Giampietro

Mastrapasqua

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Dense monolayers of living cells display intriguing relaxation dynamics, reminiscent of soft and glassy materials close to the jamming transition, and migrate collectively when space is available, as in wound healing or in cancer invasion. Here we show that collective cell migration occurs in bursts that are similar to those recorded in the propagation of cracks, fluid fronts in porous media, and ferromagnetic domain walls. In analogy with these systems, the distribution of activity bursts displays scaling laws that are universal in different cell types and for cells moving on different substrates. The main features of the invasion dynamics are quantitatively captured by a model of interacting active particles moving in a disordered landscape. Our results illustrate that collective motion of living cells is analogous to the corresponding dynamics in driven, but inanimate, systems.collective cell migration | avalanches | universality | vascular endothelial cadherin | collagen substrate C ollective cell movement depends on intracellular biological mechanisms as well as environmental cues due to the extracellular matrix (1-5), mainly composed of collagen which is organized in hierarchical structures, such as fibrils and fibers. The mechanical properties of collagen fibril networks are essential to offer little resistance and high sensitivity to small deformations, allowing easy local remodeling and strong strain stiffening needed to ensure cell and tissue integrity (6). Wound healing is a typical biological assay to study collective migration of cells under controlled conditions in vitro and is a prototypical experimental method to study active matter (7-10). Experiments performed on soluble collagen (11) or other gels (12), micropatterned (13, 14) and deformable substrates (1) show that cell migration is guided by the substrate structure and stiffness (5,15,16).It has been argued that collective migration properties arise from stresses transmitted between neighboring cells (1) giving rise to longranged stress waves in the monolayer (17,18). Hence the dynamics of an invading cell sheet is ruled by a combination of long-range internal stresses and interactions with the substrate, suggesting an analogy with driven elastic systems moving in a disordered medium such as cracks lines (19,20), imbibition fronts (21), or ferromagnetic domain walls (22). The scaling laws in these systems are usually associated with a depinning critical point that has been widely studied by simple models for interface dynamics. Thanks to a combination of numerical simulations (23, 24) and renormalization group theory (23,(25)(26)(27), we now have a detailed picture of the nonequilibrium phase transitions and universality classes in these systems. Here we substantiate the analogy between collective cell migration and depinning by revealing and characterizing widely distributed bursts of activity in the collective migration of different types of cells (human cancer cells and epithelial cells, mouse endothelial cells) over different substrates ...

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Cell and tissue mechanics in cell migration

Cited by 172 publications

References 44 publications

Simulated microgravity inhibits the migration of mesenchymal stem cells by remodeling actin cytoskeleton and increasing cell stiffness

Simulated microgravity inhibits the migration of mesenchymal stem cells by remodeling actin cytoskeleton and increasing cell stiffness

Mapping intracellular mechanics on micropatterned substrates

Bursts of activity in collective cell migration

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