Do membrane undulations help cells probe the world?

Pierrès, Anne; Monnet‐Corti, Virginie; Benoliel, Anne‐Marie; Bongrand, Pierre

doi:10.1016/j.tcb.2009.05.009

Cited by 41 publications

(44 citation statements)

References 79 publications

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“…A second conclusion concerns microvillus dynamics: the mean lifetime of contacts formed between T cells and neutral (nonadhesive, nonactivating) surfaces was 8.6 s. This is consistent with the concept that cell surfaces display spontaneous and continual protrusion/retraction processes with a characteristic time scale often ranging between 1 and 100 s (22,23,31). Adhesive interactions resulted in a .3-fold increase of this lifetime (from 8.6 to 27.6 s).…”

Section: Discussionsupporting

confidence: 82%

“…This increase may be ascribed to a combination of both passive inhibition of spontaneous retraction (by adhesive interactions) and active cell response to the adhesive force or engagement of a specific membrane receptor, which might either increase or decrease retraction. Indeed, the cell capacity to probe the mechanical properties of their surroundings has been abundantly demonstrated during the last decade (31). The key result of our study is that addition of TCR engagement to anti-HLA-mediated adhesion resulted in a 2-fold decrease of contact lifetime (from 27.6 to 13.7s).…”

Section: Discussionmentioning

confidence: 80%

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T Lymphocytes Sense Antigens within Seconds and Make a Decision within One Minute

Brodovitch

Bongrand

Pierrès

2013

The Journal of Immunology

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Adaptive immune responses are triggered by the rapid and sensitive detection of MHC-bound peptides by TCRs. The kinetics of early TCR/APC contacts are incompletely known. In this study, we used total internal reflection fluorescence microscopy to image human T cell membranes near model surfaces: contact was mediated by mobile protrusions of <0.4 μm diameter. The mean lifetime of contacts with a neutral surface was 8.6 s. Adhesive interactions increased mean contact time to 27.6 s. Additional presence of TCR ligands dramatically decreased contact to 13.7 s, thus evidencing TCR-mediated triggering of a pulling motion within seconds after ligand encounter. After an interaction typically involving 30–40 contacts formed during a 1-min observation period, TCR stimulation triggered a rapid and active cell spreading. Pulling events and cell spreading were mimicked by pharmacological phospholipase Cγ1 activation, and they were prevented by phospholipase Cγ1 inhibition. These results provide a quantitative basis for elucidating the earliest cell response to the detection of foreign Ags.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 80%

T Lymphocytes Sense Antigens within Seconds and Make a Decision within One Minute

Brodovitch

Bongrand

Pierrès

2013

The Journal of Immunology

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“…2. The characteristic traction force is assumed in the literature to be on the order of 1 nN∕μm 2 (10,28,29) and the protrusion has a typical diameter of 0.1 μm (29), comparable to the average distance between bonds (27). These estimates lead to a traction force, f 0 , on the order of 8 pN.…”

Section: Methodsmentioning

confidence: 99%

Boundary crossing in epithelial wound healing

Fong

Tzlil

Tirrell

2010

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

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The processes of wound healing and collective cell migration have been studied for decades. Intensive research has been devoted to understanding the mechanisms involved in wound healing, but the role of cell-substrate interactions is still not thoroughly understood. Here we probe the role of cell-substrate interactions by examining in vitro the healing of monolayers of human corneal epithelial (HCE) cells cultured on artificial extracellular matrix (aECM) proteins. We find that the rate of wound healing is dependent on the concentration of fibronectin-derived (RGD) cell-adhesion ligands in the aECM substrate. The wound closure rate varies nearly sixfold on the substrates examined, despite the fact that the rates of migration and proliferation of individual cells show little sensitivity to the RGD concentration (which varies 40-fold). To explain this apparent contradiction, we study collective migration by means of a dynamic Monte Carlo simulation. The cells in the simulation spread, retract, and proliferate with probabilities obtained from a simple phenomenological model. The results indicate that the overall wound closure rate is determined primarily by the rate at which cells cross the boundary between the aECM protein and the matrix deposited under the cell sheet.biomaterials | integrins | elastin T he collective migration of cells is fundamental to wound healing, morphogenesis, and many bioengineering applications. Wound healing in particular involves the migration of cell sheets over adhesive surfaces. Two mechanisms of migration have been identified in wound healing (1). First is the "purse string" mechanism in which a marginal actomyosin cable develops along the wound edge, and wound closure proceeds with contraction of the actin belt (2). The second mechanism involves active spreading and migration of cells at the wound edge, known commonly as "lamellipodial crawling." The latter mechanism is more frequently observed in vitro and has been characterized by using scratch-wound models. In these models, cells experience an injury, which triggers cell migration through various biochemical signaling events (3). It has also been argued that the availability of free space is sufficient to initiate cell migration in the absence of mechanical injury (4-6). Upon wounding, proliferation is up-regulated (7).Adhesive cell-substratum interactions are required for sustained migration into the wound area (8, 9). The rates of migration of individual cells are governed by surface adhesivity in a biphasic fashion, at least under certain conditions (10). Surfaces modified with adhesion ligands such as fibronectin (FN) (11-13) and Arg-Gly-Asp (RGD) peptides have been shown to facilitate wound healing, and it is reasonable to infer that the observed increases in healing rates arise primarily from faster migration of individual cells. We show here that other factors can be more important.The substrates used in this work were prepared from artificial extracellular matrix (aECM) proteins that combine domains derived from fibronec...

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“…63 However, there are other mechanisms affecting the cells that rely on much weaker forces. 64 Forces of a few pN can cause changes …”

Section: Amf Treatmentmentioning

confidence: 99%

Non-chemotoxic induction of cancer cell death using magnetic nanowires

Contreras¹,

Sougrat²,

Zaher³

et al. 2015

IJN

101

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In this paper, we show that magnetic nanowires with weak magnetic fields and low frequencies can induce cell death via a mechanism that does not involve heat production. We incubated colon cancer cells with two concentrations (2.4 and 12 μg/mL) of nickel nanowires that were 35 nm in diameter and exposed the cells and nanowires to an alternating magnetic field (0.5 mT and 1 Hz or 1 kHz) for 10 or 30 minutes. This low-power field exerted a force on the magnetic nanowires, causing a mechanical disturbance to the cells. Transmission electron microscopy images showed that the nanostructures were internalized into the cells within 1 hour of incubation. Cell viability studies showed that the magnetic field and the nanowires separately had minor deleterious effects on the cells; however, when combined, the magnetic field and nanowires caused the cell viability values to drop by up to 39%, depending on the strength of the magnetic field and the concentration of the nanowires. Cell membrane leakage experiments indicated membrane leakage of 20%, suggesting that cell death mechanisms induced by the nanowires and magnetic field involve some cell membrane rupture. Results suggest that magnetic nanowires can kill cancer cells. The proposed process requires simple and low-cost equipment with exposure to only very weak magnetic fields for short time periods.

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Do membrane undulations help cells probe the world?

Cited by 41 publications

References 79 publications

T Lymphocytes Sense Antigens within Seconds and Make a Decision within One Minute

T Lymphocytes Sense Antigens within Seconds and Make a Decision within One Minute

Boundary crossing in epithelial wound healing

Non-chemotoxic induction of cancer cell death using magnetic nanowires

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