scholarly journals The Biophysics of Cell Migration: Biasing Cell Motion with Feynman Ratchets

2020 ◽  
Vol 1 (2) ◽  
Author(s):  
David Caballero ◽  
Subhas C. Kundu ◽  
Rui L. Reis
Keyword(s):  
Cell Migration ◽  
Long Range ◽  
Soft Matter ◽  
Guidance Cues ◽  
Cell Locomotion ◽  
Directed Cell Migration ◽  
Laws Of Thermodynamics ◽  
Soft Matter Physics ◽  
Cell Motion

ABSTRACT The concepts and frameworks of soft matter physics and the laws of thermodynamics can be used to describe relevant developmental, physiologic, and pathologic events in which directed cell migration is involved, such as in cancer. Typically, this directionality has been associated with the presence of soluble long-range gradients of a chemoattractant, synergizing with many other guidance cues to direct the motion of cells. In particular, physical inputs have been shown to strongly influence cell locomotion. However, this type of cue has been less explored despite the importance in biology. In this paper, we describe recent in vitro works at the interface between physics and biology, showing how the motion of cells can be directed by using gradient-free environments with repeated local asymmetries. This rectification of cell migration, from random to directed, is a process reminiscent of the Feynman ratchet; therefore, this framework can be used to explain the mechanism behind directed cell motion.

A centrosomal protein FOR20 regulates microtubule assembly dynamics and plays a role in cell migration

2017 ◽  
Vol 474 (16) ◽  
pp. 2841-2859 ◽  
Author(s):  
Shalini Srivastava ◽  
Dulal Panda
Keyword(s):  
Cell Migration ◽  
Hela Cells ◽  
Growth Factor Receptor ◽  
Cell Extract ◽  
Microtubule Assembly ◽  
Igg Antibody ◽  
Centrosomal Protein ◽  
Directed Cell Migration ◽  
Associated Proteins

Here, we report that a centrosomal protein FOR20 [FOP (FGFR1 (fibroblast growth factor receptor 1) oncogene protein)-like protein of molecular mass of 20 kDa; also named as C16orf63, FLJ31153 or PHSECRG2] can regulate the assembly and stability of microtubules. Both FOR20 IgG antibody and GST (glutathione S-transferase)-tagged FOR20 could precipitate tubulin from the HeLa cell extract, indicating a possible interaction between FOR20 and tubulin. FOR20 was also detected in goat brain tissue extract and it cycled with microtubule-associated proteins. Furthermore, FOR20 bound to purified tubulin and inhibited the assembly of tubulin in vitro. The overexpression of FOR20 depolymerized interphase microtubules and the depletion of FOR20 prevented nocodazole-induced depolymerization of microtubules in HeLa cells. In addition, the depletion of FOR20 suppressed the dynamics of individual microtubules in live HeLa cells. FOR20-depleted MDA-MB-231 cells displayed zigzag motion and migrated at a slower rate than the control cells, indicating that FOR20 plays a role in directed cell migration. The results suggested that the centrosomal protein FOR20 is a new member of the microtubule-associated protein family and that it regulates the assembly and dynamics of microtubules.

scholarly journals Cortactin Promotes Migration and Platelet-derived Growth Factor-induced Actin Reorganization by Signaling to Rho-GTPases

2009 ◽  
Vol 20 (14) ◽  
pp. 3209-3223 ◽  
Author(s):  
Frank P.L. Lai ◽  
Malgorzata Szczodrak ◽  
J. Margit Oelkers ◽  
Markus Ladwein ◽  
Filippo Acconcia ◽  
...  
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Rho Gtpases ◽  
Platelet Derived Growth Factor ◽  
Actin Assembly ◽  
Actin Reorganization ◽  
Directed Cell Migration ◽  
Syndrome Protein

Dynamic actin rearrangements are initiated and maintained by actin filament nucleators, including the Arp2/3-complex. This protein assembly is activated in vitro by distinct nucleation-promoting factors such as Wiskott-Aldrich syndrome protein/Scar family proteins or cortactin, but the relative in vivo functions of each of them remain controversial. Here, we report the conditional genetic disruption of murine cortactin, implicated previously in dynamic actin reorganizations driving lamellipodium protrusion and endocytosis. Unexpectedly, cortactin-deficient cells showed little changes in overall cell morphology and growth. Ultrastructural analyses and live-cell imaging studies revealed unimpaired lamellipodial architecture, Rac-induced protrusion, and actin network turnover, although actin assembly rates in the lamellipodium were modestly increased. In contrast, platelet-derived growth factor-induced actin reorganization and Rac activation were impaired in cortactin null cells. In addition, cortactin deficiency caused reduction of Cdc42 activity and defects in random and directed cell migration. Reduced migration of cortactin null cells could be restored, at least in part, by active Rac and Cdc42 variants. Finally, cortactin removal did not affect the efficiency of receptor-mediated endocytosis. Together, we conclude that cortactin is fully dispensable for Arp2/3-complex activation during lamellipodia protrusion or clathrin pit endocytosis. Furthermore, we propose that cortactin promotes cell migration indirectly, through contributing to activation of selected Rho-GTPases.

Ratchetaxis: Long-Range Directed Cell Migration by Local Cues

2015 ◽  
Vol 25 (12) ◽  
pp. 815-827 ◽  
Author(s):  
David Caballero ◽  
Jordi Comelles ◽  
Matthieu Piel ◽  
Raphaël Voituriez ◽  
Daniel Riveline
Keyword(s):  
Cell Migration ◽  
Long Range ◽  
Directed Cell Migration ◽  
Local Cues

scholarly journals Generation of fluorescent cell-derived-matrix to study 3D cell migration

2019 ◽  
Author(s):  
Amélie Luise Godeau ◽  
Hélène Delanoë-Ayari ◽  
Daniel Riveline
Keyword(s):  
Cell Migration ◽  
Flat Surfaces ◽  
Polymeric Networks ◽  
Motile Cells ◽  
Matrix Deformation ◽  
3D Cell Migration ◽  
Cell Motion ◽  
Cellular Forces

AbstractCell migration is involved in key phenomena in biology, ranging from development to cancer. Fibroblasts move between organs in 3D polymeric networks. So far, motile cells were mainly tracked in vitro on Petri dishes or on coverslips, i.e. 2D flat surfaces, which made the extrapolation to 3D physiological environments difficult. We therefore prepared 3D Cell Derived Matrix (CDM) with specific characteristics with the goal of extracting the main readouts required to measure and characterise cell motion: cell specific matrix deformation through the tracking of fluorescent fibronectin within CDM, focal contacts as the cell anchor and acto-myosin cytoskeleton which applies cellular forces. We report our method for generating this assay of physiological-like gel with relevant readouts together with its potential impact in explaining cell motility in vivo.

5-Lipoxygenase and cyclooxygenase regulate wound closure in NIH/3T3 fibroblast monolayers

2004 ◽  
Vol 287 (2) ◽  
pp. C373-C383 ◽  
Author(s):  
J. Angelo Green ◽  
Rebecca A. Stockton ◽  
Christopher Johnson ◽  
Bruce S. Jacobson
Keyword(s):  
Cell Migration ◽  
Wound Closure ◽  
Cell Spreading ◽  
Oxidative Enzymes ◽  
Prostaglandin E ◽  
Bridge Formation ◽  
Directed Cell Migration ◽  
Cox 2 ◽  
Nih 3T3

Wound healing involves multiple cell signaling pathways, including those regulating cell-extracellular matrix adhesion. Previous work demonstrated that arachidonate oxidation to leukotriene B4 (LTB4) by 5-lipoxygenase (5-LOX) signals fibroblast spreading on fibronectin, whereas cyclooxygenase-2 (COX-2)-catalyzed prostaglandin E2 (PGE2) formation facilitates subsequent cell migration. We investigated arachidonate metabolite signaling in wound closure of perturbed NIH/3T3 fibroblast monolayers. We found that during initial stages of wound closure (0–120 min), all wound margin cells spread into the wound gap perpendicularly to the wound long axis. At regular intervals, between 120 and 300 min, some cells elongated to project across the wound and meet cells from the opposite margin, forming distinct cell bridges spanning the wound that act as foci for later wound-directed cell migration and resulting closure. 5-LOX inhibition by AA861 demonstrated a required LTB4 signal for initial marginal cell spreading and bridge formation, both of which must precede wound-directed cell migration. 5-LOX inhibition effects were reversible by exogenous LTB4. Conversely, COX inhibition by indomethacin reduced directed migration into the wound but enhanced early cell spreading and bridge formation. Exogenous PGE2 reversed this effect and increased cell migration into the wound. The differential effects of arachidonic acid metabolites produced by LOX and COX were further confirmed with NIH/3T3 fibroblast cell lines constitutively over- and underexpressing the 5-LOX and COX-2 enzymes. These data suggest that two competing oxidative enzymes in arachidonate metabolism, LOX and COX, differentially regulate sequential aspects of fibroblast wound closure in vitro.

Expression of tenascin in response to neural induction in amphibian embryos

Development ◽  
1988 ◽  
Vol 104 (3) ◽  
pp. 511-524 ◽  
Author(s):  
J.-F. Riou ◽  
D.-L. Shi ◽  
M. Chiquet ◽  
J.-C. Boucaut
Keyword(s):  
Cell Migration ◽  
Neural Crest Cell ◽  
Neural Induction ◽  
Gastrula Stage ◽  
Directed Cell Migration ◽  
Pleurodeles Waltl ◽  
Migration Pathways ◽  
Early Gastrula

The expression of tenascin, a constituent of extracellular matrix (ECM), was studied during the embryonic development of the amphibian Pleurodeles waltl. An antiserum to chick fibroblast tenascin was shown to cross-react with the homologous molecule of the amphibian. Immunostaining of embryo sections with anti-tenascin antiserum revealed that tenascin appears just after the completion of neurulation. At the tailbud stage, tenascin is present in the ECM located at sites of directed cell migration (neural crest cell migration pathways, extension of the pronephretic duct) and mesenchyme condensation (endocardium, aortic arches). The accumulation of tenascin immunoreactivity in the embryonic ECM is correlated with the synthesis of the 220×103Mr polypeptide of the molecule. To provide data on the patterning of tenascin, ectoderm and dorsal blastoporal lip isolated at early gastrula stage were cultured for a period of 3 days. Epidermal vesicles differentiating from isolated ectoderm completely lack tenascin. Conversely, axial mesoderm derivatives present in cultured dorsal blastoporal lip were found to produce tenascin. Neural induction of ectoderm isolated at early gastrula stage was performed in vitro with the dorsal blastoporal lip or concanavalin A. The induced neural tissue was found to accumulate tenascin. Spemann experiments confirmed in vivo that tenascin is expressed by ectodermal cells as a response to neural induction.

scholarly journals Collagen fibers provide guidance cues for capillary regrowth during regenerative angiogenesis in zebrafish

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anita Senk ◽  
Valentin Djonov
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Collagen Scaffold ◽  
Collagen Iv ◽  
Collagen Fibers ◽  
Collagen I ◽  
Endothelial Cell Migration ◽  
In Vitro Assays ◽  
Guidance Cues

AbstractAlthough well investigated, the importance of collagen fibers in supporting angiogenesis is not well understood. In this study, we demonstrate that extracellular collagen fibers provide guidance cues for endothelial cell migration during regenerative angiogenesis in the caudal zebrafish fin. Inhibition of collagen cross-linking by β-Aminopropionitrile results in a 70% shorter regeneration area with 50% reduced vessel growth and disintegrated collagen fibers. The disrupted collagen scaffold impedes endothelial cell migration and induces formation of abnormal angioma-like blood vessels. Treatment of the Fli//colRN zebrafish line with the prodrug Nifurpirinol, which selectively damages the active collagen-producing 1α2 cells, reduced the regeneration area and vascular growth by 50% with wider, but less inter-connected, capillary segments. The regenerated area contained larger vessels partially covered by endothelial cells embedded in atypical extracellular matrix containing cell debris and apoptotic bodies, macrophages and granulocytes. Similar experiments performed in early embryonic zebrafish suggested that collagens are important also during embryonic angiogenesis. In vitro assays revealed that collagen I allows for the most efficient endothelial cell migration, followed by collagen IV relative to the complete absence of exogenous matrix support. Our data demonstrates severe vascular defects and restricted fin regeneration when collagens are impaired. Collagen I therefore, provides support and guidance for endothelial cell migration while collagen IV is responsible for proper lumen formation and vascular integrity.

Neutrophil migration through in vitro interstitial matrix

1992 ◽  
Vol 50 (1) ◽  
pp. 894-895
Author(s):  
J. Roemer ◽  
S.R. Simon
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Cells ◽  
Inflammatory Cell ◽  
Neutrophil Migration ◽  
Culture Conditions ◽  
Aortic Smooth Muscle ◽  
Specific Culture

We are developing an in vitro interstitial extracellular matrix (ECM) system for study of inflammatory cell migration. Falcon brand Cyclopore membrane inserts of various pore sizes are used as a support substrate for production of ECM by R22 rat aortic smooth muscle cells. Under specific culture conditions these cells produce a highly insoluble matrix consisting of typical interstitial ECM components, i.e.: types I and III collagen, elastin, proteoglycans and fibronectin.

The Migration of Human Smooth Muscle Cells In Vitro Is Mediated by Plasminogen Activation and Can Be Inhibited by α2-Macroglobulin Receptor Associated Protein

1997 ◽  
Vol 78 (02) ◽  
pp. 880-886 ◽  
Author(s):  
Monique J Wijnberg ◽  
Paul H A Quax ◽  
Nancy M E Nieuwenbroek ◽  
Jan H Verheijen
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Ldl Receptor ◽  
Migration And Invasion ◽  
Invasion Assay ◽  
Plasminogen Activation ◽  
Smooth Muscle Cell Migration

SummaryThe plasminogen activation system is thought to be important in cell migration processes. A role for this system during smooth muscle cell migration after vascular injury has been suggested from several animal studies. However, not much is known about its involvement in human vascular remodelling. We studied the involvement of the plasminogen activation system in human smooth muscle cell migration in more detail using an in vitro wound assay and a matrix invasion assay. Inhibition of plasmin activity or inhibition of urokinase-type plasminogen activator (u-PA) activity resulted in approximately 40% reduction of migration after 24 h in the wound assay and an even stronger reduction (70-80%) in the matrix invasion assay. Migration of smooth muscle cells in the presence of inhibitory antibodies against tissue-type plasminogen activator (t-PA) was not significantly reduced after 24 h, but after 48 h a 30% reduction of migration was observed, whereas in the matrix invasion assay a 50% reduction in invasion was observed already after 24 h. Prevention of the interaction of u-PA with cell surface receptors by addition of soluble u-PA receptor or α2-macroglobulin receptor associated protein (RAP) to the culture medium, resulted in a similar inhibition of migration and invasion. From these results it can be concluded that both u-PA and t-PA mediated plasminogen activation can contribute to in vitro human smooth muscle cell migration and invasion. Furthermore, the interaction between u-PA and its cell surface receptor appears also to be involved in this migration and invasion process. The inhibitory effects on migration and invasion by the addition of RAP suggests an involvement of a RAP sensitive receptor of the LDL receptor family, possibly the LDL-receptor related protein (LRP) and/or the VLDL receptor.

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