Interaction forces between red cells agglutinated by antibody. III. Micromanipulation

Tha, S.P.; Goldsmith, Harry L.

doi:10.1016/s0006-3495(88)83149-7

Cited by 14 publications

(8 citation statements)

References 34 publications

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“…The nature of inter-cellular forces in the two situations is quite different. For two attached cells sheared in dilute suspension (which approximates the situation here when a rosette is first forming) the normal force between the cells alternates between compression (pushing them together) and extension as they rotate around each other in the shear flow, with a superimposed periodic tangential shearing force between the cells (Tha & Goldsmith, 1986). The maximal disruptive normal or shear force can be calculated to be about 10 ¹10 N at a shear stress of 1·0 Pa for two spherical cells of diameter 6 mm (i.e.…”

Section: Discussionmentioning

confidence: 99%

Rheological analysis of the formation of rosettes by red blood cells parasitized by Plasmodium falciparum

1997

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Red blood cells infected by mature malarial parasites of the species Plasmodium falciparum can adhere to non-parasitized red cells (rosetting) and also to endothelial cells (cytoadhesion). To investigate how the circulation might influence rosetting, we studied formation of rosettes in cell suspensions sheared in a cone-and-plate viscometer, and the ability of flowing non-parasitized cells to bind to parasitized cells already adherent to a surface. After rosettes of strain R29 had been disrupted with fucoidan, they reformed slowly under stationary conditions but more rapidly in suspensions sheared at low stress (about 0.1-0.2 Pa). Strain Malayan Camp gave a lower rosetting frequency which actually increased at low shear. Increasing shear stress was associated with reduction in rosette formation, although rosetting occurred at >1 Pa, suggesting that rosettes could form in the systemic circulation. Rosetting inhibited adhesion of flowing parasitized cells to immobilized platelets (which express the cytoadhesion receptor CD36), as evidenced by increased adhesion after disruption of rosettes. The de-rosetted adherent cells parasitized by R29 supported only a low level of rosetting when non-parasitized cells were flowed over them at a wall shear of 0.1 Pa, with little increase if the stress was decreased to 0.05 Pa. Rosettes formed in the circulation might obstruct microvessels and inhibit cytoadhesion if they reached venules. However, if cytoadhesion occurred before rosetting, then adherent cells should not efficiently form rosettes.

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Section: Discussionmentioning

confidence: 99%

Rheological analysis of the formation of rosettes by red blood cells parasitized by Plasmodium falciparum

1997

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“…The forces required to rupture an adhesive bond or extract a receptor from the lipid bilayer have either been measured or estimated and are in the vicinity of 1 ,udyn (Evans et al, 1991;Tha and Goldsmith, 1988;Bell, 1978). For an adhesive spring, comparable forces are obtained for values of lb and Is such that (lb X)2/212 3 to 5.…”

Section: General Adhesion Model (No Focal Contacts)mentioning

confidence: 99%

A theoretical analysis for the effect of focal contact formation on cell-substrate attachment strength

Ward

Hammer

1993

Biophysical Journal

143

106

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For many cell types, growth, differentiation, and motility are dependent on receptor-mediated adhesion to ligand-coated surfaces. Focal contacts are strong, specialized, adhesive connections between cell and substrate in which receptors aggregate and connect extracellular ligand to intracellular cytoskeletal molecules. In this paper, we present a mathematical model to examine how focal contact formation affects cellular adhesive strength. To calculate adhesive strength with and without focal contacts, we use a one-dimensional tape peeling analysis to determine the critical tension necessary to peel the membrane. Receptor-ligand bonds are modeled as adhesive springs. In the absence of focal contacts, we derive analytic expressions for the critical tension at low and high ligand densities and show how membrane morphology affects adhesion. Then, focal contacts are modeled as cytoplasmic nucleation centers which bind adhesion receptors. The extent of adhesive strengthening upon focal contact formation depends on the elastic rigidity of the cytoskeletal connections, which determines the structural integrity of the focal contact itself. We consider two limits to this elasticity, very weak and rigid. Rigid cytoskeletal connections give much greater attachment strengths. The dependence of attachment strength on measurable model parameters is quite different in these two limits, which suggests focal contact structure might be deduced from properly performed adhesion experiments. Finally, we compare our model to the adhesive strengthening response reported for glioma cell adhesion to fibronectin (Lotz et al., 1989. J. Cell Biol. 109:1795-1805). Our model successfully predicts the observed detachment forces at 4 degrees C and yields values for the number of fibronectin receptors per glioma cell and the density of cytoskeletal connection molecules (talin) involved in receptor clusters which are consistent with measurements for other cell types. Comparison of the model with data at 37 degrees C suggests that while cytoskeletal cross-linking and clustering of fibronectin receptors significantly increases adhesion strength, specific glioma cell-substratum attachment sites possess little mechanical rigidity and detach through a peeling mechanism, consistent with the view that these sites of < or = 15 nm cell-substrate separation are precursors to fully formed, elastically rigid focal contacts.

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“…25 Adhesive failure will be significant when the bond density and the area to perimeter ratio are small. Using the estimated bond forces (Table II) and the force to extract receptors through the membrane (1 dyne) 26,27 the ratio f b AN b L/f mem P c was less than one only for the surface with the highest HEMA content. If, however, cohesive failure truly is occurring, it would not be possible to measure the intrinsic bond forces of the magnitude reported.…”

Section: Discussionmentioning

confidence: 99%

Role of endothelial cell-substrate contact area and fibronectin-receptor affinity in cell adhesion to HEMA/EMA copolymers

Burmeister

McKinney

Reichert

et al. 1999

J. Biomed. Mater. Res.

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The objective of this study was to examine the effect of substrate hydrophobicity on cell-substrate contact area and the affinity between adsorbed fibronectin (Fn) and its receptor. Homo- and copolymer films of hydrophobic ethyl methacrylate (EMA) and hydrophilic hydroxyethyl methacrylate (HEMA) were spun-cast onto glass slides. Bovine aortic endothelial cells (BAEC) were plated for 2 h in serum-free medium onto polymers preadsorbed with Fn. Cells were fixed, labeled, and examined by total internal reflection fluorescence microscopy (TIRFM) to determine the topography of the basal surface as a function of distance from the substrate. Phase contrast microscopy was used to examine the total projected area of adherent cells. The cumulative contact area was greatest on cells attached to surfaces prepared from 0% HEMA and lowest on surfaces with the highest HEMA content. An equilibrium adhesion model used these data together with the critical force for detachment and the Fn density (Burmeister et al., J Biomed Mater Res 1996;30:13-22) to determine the affinity between Fn and its receptor and the bond strength. The affinity and force per bond decreased with increasing HEMA content. These results indicate that differences in the strength of endothelial cell adhesion to polymers are influenced by the conformation of the adsorbed adhesion proteins.

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Interaction forces between red cells agglutinated by antibody. III. Micromanipulation

Cited by 14 publications

References 34 publications

Rheological analysis of the formation of rosettes by red blood cells parasitized by Plasmodium falciparum

Rheological analysis of the formation of rosettes by red blood cells parasitized by Plasmodium falciparum

A theoretical analysis for the effect of focal contact formation on cell-substrate attachment strength

Role of endothelial cell-substrate contact area and fibronectin-receptor affinity in cell adhesion to HEMA/EMA copolymers

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