scholarly journals Physical limits of cell migration: Control by ECM space and nuclear deformation and tuning by proteolysis and traction force

2013 ◽  
Vol 201 (7) ◽  
pp. 1069-1084 ◽  
Author(s):  
Katarina Wolf ◽  
Mariska te Lindert ◽  
Marina Krause ◽  
Stephanie Alexander ◽  
Joost te Riet ◽  
...  
Keyword(s):  
Cell Migration ◽  
Interstitial Cell ◽  
Proteolytic Enzymes ◽  
Traction Force ◽  
Nuclear Deformation ◽  
Cell Deformability ◽  
Migration Rates ◽  
Nuclear Cross Section ◽  
Space Restriction ◽  
Collagen Lattices

Cell migration through 3D tissue depends on a physicochemical balance between cell deformability and physical tissue constraints. Migration rates are further governed by the capacity to degrade ECM by proteolytic enzymes, particularly matrix metalloproteinases (MMPs), and integrin- and actomyosin-mediated mechanocoupling. Yet, how these parameters cooperate when space is confined remains unclear. Using MMP-degradable collagen lattices or nondegradable substrates of varying porosity, we quantitatively identify the limits of cell migration by physical arrest. MMP-independent migration declined as linear function of pore size and with deformation of the nucleus, with arrest reached at 10% of the nuclear cross section (tumor cells, 7 µm2; T cells, 4 µm2; neutrophils, 2 µm2). Residual migration under space restriction strongly depended upon MMP-dependent ECM cleavage by enlarging matrix pore diameters, and integrin- and actomyosin-dependent force generation, which jointly propelled the nucleus. The limits of interstitial cell migration thus depend upon scaffold porosity and deformation of the nucleus, with pericellular collagenolysis and mechanocoupling as modulators.

scholarly journals Different Cell Migration Modes: Insights from Traction Force Microscopy and Modeling

2021 ◽  
Vol 120 (3) ◽  
pp. 113a
Author(s):  
Wouter-Jan Rappel ◽  
Elisabeth Ghabache ◽  
Yuansheng Cao ◽  
Yuchuan Miao ◽  
Alexander Groisman ◽  
...  
Keyword(s):  
Cell Migration ◽  
Traction Force ◽  
Traction Force Microscopy ◽  
Force Microscopy

Cell-extracellular matrix interactions under in vivo conditions during interstitial cell migration in Hydra vulgaris

Development ◽  
1994 ◽  
Vol 120 (2) ◽  
pp. 425-432 ◽  
Author(s):  
X. Zhang ◽  
M.P. Sarras
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Synthetic Peptide ◽  
Interstitial Cell ◽  
Extracellular Matrix Components ◽  
Matrix Interactions ◽  
Apical Half ◽  
Matrix Components ◽  
Extracellular Matrix Interactions

Interstitial cell (I-cell) migration in hydra is essential for establishment of the regional cell differentiation pattern in the organism. All previous in vivo studies have indicated that cell migration in hydra is a result of cell-cell interactions and chemotaxic gradients. Recently, in vitro cell adhesion studies indicated that isolated nematocytes could bind to substrata coated with isolated hydra mesoglea, fibronectin and type IV collagen. Under these conditions, nematocytes could be observed to migrate on some of these extracellular matrix components. By modifying previously described hydra grafting techniques, two procedures were developed to test specifically the role of extracellular matrix components during in vivo I-cell migration in hydra. In one approach, the extracellular matrix structure of the apical half of the hydra graft was perturbed using beta-aminopropionitrile and beta-xyloside. In the second approach, grafts were treated with fibronectin, RGDS synthetic peptide and antibody to fibronectin after grafting was performed. In both cases, I-cell migration from the basal half to the apical half of the grafts was quantitatively analyzed. Statistical analysis indicated that beta-aminopropionitrile, fibronectin, RGDS synthetic peptide and antibody to fibronectin all were inhibitory to I-cell migration as compared to their respective controls. beta-xyloside treatment had no effect on interstitial cell migration. These results indicate the potential importance of cell-extracellular matrix interactions during in vivo I-cell migration in hydra.

scholarly journals Amikacin Suppresses Human Breast Cancer Cell MDA-MB-231 Migration and Invasion

Toxics ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 108
Author(s):  
Yun-Hsin Wang ◽  
Yau-Hung Chen ◽  
Wen-Hao Shen
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Western Blotting ◽  
Bacterial Infections ◽  
Aminoglycoside Antibiotic ◽  
Migration And Invasion ◽  
Interacting Protein ◽  
Migration Rates ◽  
Thioredoxin Interacting Protein ◽  
Sirna Knockdown

(1) Background: Amikacin is an aminoglycoside antibiotic used for treating gram-negative bacterial infections in cancer patients. In this study, our aims are to investigate the migratory inhibition effects of amikacin in human MDA-MB-231 cells. (2) Methods: We used a wound-healing assay, trans-well analysis, Western blotting, immunostaining and siRNA knockdown approaches to investigate how amikacin influenced MDA-MB-231 cell migration and invasion. (3) Results: Wound healing showed that the MDA-MB-231 cell migration rates decreased to 44.4% in the presence of amikacin. Trans-well analysis showed that amikacin treatment led to invasion inhibition. Western blotting demonstrated that amikacin induced thioredoxin-interacting protein (TXNIP) up-regulation. TXNIP was knocked down using siRNA in MDA-MB-231 cell. Using immunostaining analysis, we found that inhibition of TXNIP expression led to MDA-MB-231 pseudopodia extension; however, amikacin treatment attenuated the cell extension formation. (4) Conclusions: We observed inhibition of migration and invasion in MDA-MB-231 cells treated with amikacin. This suggests inhibition might be mediated by up-regulation of TXNIP.

scholarly journals Grip and slip of L1-CAM on adhesive substrates direct growth cone haptotaxis

2018 ◽  
Vol 115 (11) ◽  
pp. 2764-2769 ◽  
Author(s):  
Kouki Abe ◽  
Hiroko Katsuno ◽  
Michinori Toriyama ◽  
Kentarou Baba ◽  
Tomoyuki Mori ◽  
...  
Keyword(s):  
Cell Migration ◽  
Growth Cone ◽  
Cell Adhesion Molecule ◽  
Chemical Cues ◽  
Traction Force ◽  
Human Patient ◽  
Direct Growth ◽  
Direct Cell ◽  
Conventional Cell ◽  
Directional Cell Migration

Chemical cues presented on the adhesive substrate direct cell migration, a process termed haptotaxis. To migrate, cells must generate traction forces upon the substrate. However, how cells probe substrate-bound cues and generate directional forces for migration remains unclear. Here, we show that the cell adhesion molecule (CAM) L1-CAM is involved in laminin-induced haptotaxis of axonal growth cones. L1-CAM underwent grip and slip on the substrate. The ratio of the grip state was higher on laminin than on the control substrate polylysine; this was accompanied by an increase in the traction force upon laminin. Our data suggest that the directional force for laminin-induced growth cone haptotaxis is generated by the grip and slip of L1-CAM on the substrates, which occur asymmetrically under the growth cone. This mechanism is distinct from the conventional cell signaling models for directional cell migration. We further show that this mechanism is disrupted in a human patient with L1-CAM syndrome, suffering corpus callosum agenesis and corticospinal tract hypoplasia.

Site determination and application of LTBP-1, a molecule related to atherosclerosis, involved in cell migration

Impact ◽  
2021 ◽  
Vol 2021 (6) ◽  
pp. 24-25
Author(s):  
Seisuke Mimori
Keyword(s):  
Coronary Artery Disease ◽  
Cell Migration ◽  
Coronary Artery ◽  
Mechanism Of Action ◽  
Clinical Medicine ◽  
Associate Professor ◽  
Migration Rates ◽  
Artery Disease ◽  
The Impact ◽  
Underlying Processes

The two strands of treatment available for coronary artery disease and associated pathologies are pharmaceutical and physical. However, these treatments are typically only available too late to help tackle the early underlying processes. Better understanding of the underlying processes is key to the development of preventative solutions. One of the key processes understanding coronary problems is atherosclerosis, which is when arteries lose elasticity. Associate Professor Seisuke Mimori, Department of Clinical Medicine, Chiba Institute of Science, Japan, is examining the underlying biochemistry of atherosclerosis. Professor Tetsuto Kanzaki has succeeded in cloning a protein called LTBP-1 and, under his direction, Seisuke has created a mutant of the protein and is analysing it. He intends to produce variants of LTBP-1 in order to investigate the function of various domains of the protein. This will involve firstly producing and isolating the protein and its variants in sufficient quantities. Then, he will test cell migration rates through an assay that he and the team have designed. This will enable the researchers to clarify exactly how LTBP-1 functions. In the future, Seisuke and the team will investigate the exact mechanism of action of the domains involved and explore the impact of LTBP-1 on the relevant organs and cells.

scholarly journals Open source software for quantification of cell migration, protrusions, and fluorescence intensities

2015 ◽  
Vol 209 (1) ◽  
pp. 163-180 ◽  
Author(s):  
David J. Barry ◽  
Charlotte H. Durkin ◽  
Jasmine V. Abella ◽  
Michael Way
Keyword(s):  
Cell Migration ◽  
Open Source ◽  
Imaging Techniques ◽  
Automated Analysis ◽  
Spatial And Temporal Scales ◽  
Migration Rates ◽  
Automated Quantification ◽  
Membrane Protrusions ◽  
Automated Tools ◽  
User Friendly

Cell migration is frequently accompanied by changes in cell morphology (morphodynamics) on a range of spatial and temporal scales. Despite recent advances in imaging techniques, the application of unbiased computational image analysis methods for morphodynamic quantification is rare. For example, manual analysis using kymographs is still commonplace, often caused by lack of access to user-friendly, automated tools. We now describe software designed for the automated quantification of cell migration and morphodynamics. Implemented as a plug-in for the open-source platform, ImageJ, ADAPT is capable of rapid, automated analysis of migration and membrane protrusions, together with associated fluorescently labeled proteins, across multiple cells. We demonstrate the ability of the software by quantifying variations in cell population migration rates on different extracellular matrices. We also show that ADAPT can detect and morphologically profile filopodia. Finally, we have used ADAPT to compile an unbiased description of a “typical” bleb formed at the plasma membrane and quantify the effect of Arp2/3 complex inhibition on bleb retraction.

Interstitial cell migration in Hydra attenuata

1984 ◽  
Vol 105 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Shelly Heimfeld ◽  
Hans R. Bode
Keyword(s):  
Cell Migration ◽  
Interstitial Cell ◽  
Hydra Attenuata
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