scholarly journals Guiding 3D cell migration in deformed synthetic hydrogel microstructures

Soft Matter ◽  
2018 ◽  
Vol 14 (15) ◽  
pp. 2816-2826 ◽  
Author(s):  
Miriam Dietrich ◽  
Hugo Le Roy ◽  
David B. Brückner ◽  
Hanna Engelke ◽  
Roman Zantl ◽  
...  
Keyword(s):  
Cell Migration ◽  
Theoretical Modelling ◽  
Synthetic Hydrogel ◽  
3D Cell Migration ◽  
External Strain ◽  
Migration Response

In this study we combine experiments and theoretical modelling to analyse the anisotropic migration response of cells to external strain.

scholarly journals Combinative in vitro studies and computational model to predict 3D cell migration response to drug insult

2014 ◽  
Vol 6 (10) ◽  
pp. 957-972 ◽  
Author(s):  
Joseph S. Maffei ◽  
Jaya Srivastava ◽  
Brian Fallica ◽  
Muhammad H. Zaman
Keyword(s):  
Cell Migration ◽  
Computational Model ◽  
In Vitro Studies ◽  
3D Cell Migration ◽  
Migration Response

Nucleus and nucleus-cytoskeleton connections in 3D cell migration

2016 ◽  
Vol 348 (1) ◽  
pp. 56-65 ◽  
Author(s):  
Lingling Liu ◽  
Qing Luo ◽  
Jinghui Sun ◽  
Guanbin Song
Keyword(s):  
Cell Migration ◽  
3D Cell Migration

A Microfluidic Assay for Metastasis Potential Analysis

2010 ◽  
Author(s):  
Smitha M. N. Rao ◽  
Uday Tata ◽  
Victor K. Lin ◽  
Jer-Tsong Hsieh ◽  
Kytai Nguyen ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Progression ◽  
Soft Lithography ◽  
Microfluidic Devices ◽  
Time Lapse ◽  
Microfluidic Channels ◽  
Control Groups ◽  
Dimethyl Siloxane ◽  
Microfluidic Assays ◽  
Migration Response

We have designed and characterized a poly-dimethyl-siloxane (PDMS) based microfluidic device called MiMiC™ that enables time-lapse study of cell migration. Cell migration is a key step of malignant metastasis during cancer progression. The device mimics the narrow confines the cells need to traverse and the microenvironments that are similar to the ones inside human body. Photolithography and soft lithography processes were used to fabricate the microfluidic devices. The device consists of two separate chambers connected by microfluidic channels allowing introduction of cells in one chamber and chemoattractants in the other. The response of lung-metastasized prostate cancer (PC-3-ML) cells and their migration response to chemoattractants were observed and analyzed. The numbers of cells under migration were determined from time-lapse images and compared to control groups. Our microfluidic assays provide advantages over the traditional Boyden chambers such as time-lapse observation, use of smaller amounts of reagents and direct assessment of cells under migration.

scholarly journals Myosin IIA Dependent Retrograde Flow Drives 3D Cell Migration

2010 ◽  
Vol 98 (8) ◽  
pp. L29-L31 ◽  
Author(s):  
Wenting Shih ◽  
Soichiro Yamada
Keyword(s):  
Cell Migration ◽  
Retrograde Flow ◽  
Myosin Iia ◽  
3D Cell Migration

scholarly journals Nonpolarized signaling reveals two distinct modes of 3D cell migration

2012 ◽  
Vol 197 (3) ◽  
pp. 439-455 ◽  
Author(s):  
Ryan J. Petrie ◽  
Núria Gavara ◽  
Richard S. Chadwick ◽  
Kenneth M. Yamada
Keyword(s):  
Cell Migration ◽  
Intracellular Signaling ◽  
Myosin Ii ◽  
Three Dimensional ◽  
Leading Edge ◽  
Elastic Behavior ◽  
Collagen Gels ◽  
Primary Fibroblasts ◽  
Context Specific ◽  
3D Cell Migration

We search in this paper for context-specific modes of three-dimensional (3D) cell migration using imaging for phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and active Rac1 and Cdc42 in primary fibroblasts migrating within different 3D environments. In 3D collagen, PIP3 and active Rac1 and Cdc42 were targeted to the leading edge, consistent with lamellipodia-based migration. In contrast, elongated cells migrating inside dermal explants and the cell-derived matrix (CDM) formed blunt, cylindrical protrusions, termed lobopodia, and Rac1, Cdc42, and PIP3 signaling was nonpolarized. Reducing RhoA, Rho-associated protein kinase (ROCK), or myosin II activity switched the cells to lamellipodia-based 3D migration. These modes of 3D migration were regulated by matrix physical properties. Specifically, experimentally modifying the elasticity of the CDM or collagen gels established that nonlinear elasticity supported lamellipodia-based migration, whereas linear elasticity switched cells to lobopodia-based migration. Thus, the relative polarization of intracellular signaling identifies two distinct modes of 3D cell migration governed intrinsically by RhoA, ROCK, and myosin II and extrinsically by the elastic behavior of the 3D extracellular matrix.

scholarly journals Controlled architectural and chemotactic studies of 3D cell migration

Biomaterials ◽  
2011 ◽  
Vol 32 (10) ◽  
pp. 2634-2641 ◽  
Author(s):  
Prakriti Tayalia ◽  
Eric Mazur ◽  
David J. Mooney
Keyword(s):  
Cell Migration ◽  
3D Cell Migration

scholarly journals One-dimensional topography underlies three-dimensional fibrillar cell migration

2009 ◽  
Vol 184 (4) ◽  
pp. 481-490 ◽  
Author(s):  
Andrew D. Doyle ◽  
Francis W. Wang ◽  
Kazue Matsumoto ◽  
Kenneth M. Yamada
Keyword(s):  
Cell Culture ◽  
Extracellular Matrix ◽  
Cell Migration ◽  
Myosin Ii ◽  
Three Dimensional ◽  
Two Dimensional ◽  
Ligand Density ◽  
One Dimensional ◽  
3D Cell Migration ◽  
Striking Contrast

Current concepts of cell migration were established in regular two-dimensional (2D) cell culture, but the roles of topography are poorly understood for cells migrating in an oriented 3D fibrillar extracellular matrix (ECM). We use a novel micropatterning technique termed microphotopatterning (μPP) to identify functions for 1D fibrillar patterns in 3D cell migration. In striking contrast to 2D, cell migration in both 1D and 3D is rapid, uniaxial, independent of ECM ligand density, and dependent on myosin II contractility and microtubules (MTs). 1D and 3D migration are also characterized by an anterior MT bundle with a posterior centrosome. We propose that cells migrate rapidly through 3D fibrillar matrices by a 1D migratory mechanism not mimicked by 2D matrices.

scholarly journals Mechanotransduction of fluid stresses governs 3D cell migration

2014 ◽  
Vol 111 (7) ◽  
pp. 2447-2452 ◽  
Author(s):  
W. J. Polacheck ◽  
A. E. German ◽  
A. Mammoto ◽  
D. E. Ingber ◽  
R. D. Kamm
Keyword(s):  
Cell Migration ◽  
3D Cell Migration

scholarly journals Computational estimates of mechanical constraints on cell migration through the extracellular matrix

2020 ◽  
Author(s):  
Ondrej Maxian ◽  
Alex Mogilner ◽  
Wanda Strychalski
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Pressure Gradient ◽  
Cell Body ◽  
Fluid Pressure ◽  
Three Dimensional ◽  
Extracellular Fluid ◽  
Cell Cortex ◽  
3D Cell Migration ◽  
Parameter Values

AbstractCell migration through a three-dimensional (3D) extracellular matrix (ECM) underlies important physiological phenomena and is based on a variety of mechanical strategies depending on the cell type and the properties of the ECM. By using computer simulations, we investigate two such migration mechanisms – ‘push-pull’ (forming a finger-like protrusion, adhering to an ECM node, and pulling the cell body forward) and ‘rear-squeezing’ (pushing the cell body through the ECM by contracting the cell cortex and ECM at the cell rear). We present a computational model that accounts for both elastic deformation and forces of the ECM, an active cell cortex and nucleus, and for hydrodynamic forces and flow of the extracellular fluid, cytoplasm and nucleoplasm. We find that relations between three mechanical parameters – the cortex’s contractile force, nuclear elasticity and ECM rigidity – determine the effectiveness of cell migration through the dense ECM. The cell can migrate persistently even if its cortical contraction cannot deform a near-rigid ECM, but then the contraction of the cortex has to be able to sufficiently deform the nucleus. The cell can also migrate even if it fails to deform a stiff nucleus, but then it has to be able to sufficiently deform the ECM. Simulation results show that nuclear stiffness limits the cell migration more than the ECM rigidity. Simulations of the rear-squeezing mechanism of motility results in more robust migration with larger cell displacements than those with the push-pull mechanism over a range of parameter values.Author summaryComputational simulations of models representing two different mechanisms of 3D cell migration in an extracellular matrix are presented. One mechanism represents a mesenchymal mode, characterized by finger-like actin protrusions, while the second mode is more amoeboid in that rear contraction of the cortex propels the cell forward. In both mechanisms, the cell generates a thin actin protrusion on the cortex that attaches to an ECM node. The cell is then either pulled (mesenchymal) or pushed (amoeboid) forward. Results show both mechanisms result in successful migration over a range of simulated parameter values as long as the contractile tension of the cortex exceeds either the nuclear stiffness or ECM stiffness, but not necessarily both. However, the distance traveled by the amoeboid migration mode is more robust to changes in parameter values, and is larger than in simulations of the mesenchymal mode. Additionally cells experience a favorable fluid pressure gradient when migrating in the amoeboid mode, and an adverse fluid pressure gradient in the mesenchymal mode.

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