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Biomedical subjects

E L Elson

Publications and source records attributed to E L Elson.

At least 73 records · Page 4Linked to original sources
PubMed1984

Cross-linking surface immunoglobulin increases the stiffness of lymphocytes.

Cross-linking surface immunoglobulin (sIg) on B-lymphocytes causes a substantial increase in the mechanical stiffness of the cells. This has been demonstrated using a new method for measuring cellular deformability. The method is based on a device, the "Cell Poker", which we use to determine the force required slightly to indent or compress a cell adherent to a rigid substrate in culture. Cross-linking of sIg by bivalent anti-sIg antibodies is necessary to elicit the increase in stiffness; binding of monovalent Fab fragments is insufficient. The increase in stiffness is partially reversed by cytochalasin D and by completion of the capping of the cross-linked sIg. The modulation of cellular deformability and the induction of cellular dynamic processes such as capping are similar in their requirements for cross-linking sIg and in their sensitivity to cytochalasins. This suggests that both kinds of responses stem from similar cellular processes and structures. These results emphasize the mechanical capability of lymphocytes and suggest that the physiological functions of these cells are likely to employ this capability.

Animals↗
PubMed1984

Cell poking. Determination of the elastic area compressibility modulus of the erythrocyte membrane.

Cell poking, a new method for measuring mechanical properties of single cells was used to determine the elastic area compressibility modulus of osmotically swollen human erythrocytes. With this method we determined the force required to indent cells attached to a glass coverslip (Petersen, N.O., W. B. McConnaughey , and E. L. Elson , 1982, Proc. Natl. Acad. Sci. USA, 79:5327. Forces on the order of one millidyne and indentations on the order of one micron were detected. An analysis of these data in terms of a simplified mechanical model yielded the elastic area compressibility modulus. This analysis used a variational approach to minimize the isothermal elastic potential energy density function given by E. A. Evans and R. Skalak (Mechanics and Thermodynamics of Biomembranes, 1980, CRC Press, Boca Raton , FL). Measurements on swollen erythrocytes gave a range of values, depending in part on the osmotic conditions, of 17.9 +/- 8.2 to 34.8 +/- 12.0 mdyn /micron for the elastic area compressibility modulus at 25 degrees C. Fractional area expansion greater than 2.6 +/- 0.8% produced rapid cell lysis. These values were not corrected for the reversible movement of water across the cell membrane in response to hydrostatic pressure gradients. Our results agree reasonably with those obtained by Evans et al. (Evans, E.A., R. Waugh , and L. Melnick , 1976, Biophys. J., 16:585-595.) using micropipette aspiration under similar conditions.

Elasticity↗
PubMed1982

Dependence of locally measured cellular deformability on position on the cell, temperature, and cytochalasin B.

We describe an approach to exploring cell surface-cytoskeleton interactions through direct measurements of the mechanical resistance of living cells to locally applied forces. These measurements are sensitive to variations in structure across the cell and at various depths below its surface. We find that local cellular deformability depends on the temperature and on the integrity of the cytoskeleton. Cytochalasin B increases the deformability of all regions of the cell except the nucleus.

Animals↗
PubMed1982

Lateral motion of beta receptors in membranes of cultured liver cells.

We have studied the lateral mobility and distribution of beta receptors on Chang human liver cells by fluorescence photobleaching recovery and video intensification microscopy. The beta receptors were labeled with the fluorescent antagonist 7-(2-allylphenoxy)-2,2-dimethyl-6-hydroxy-1-(4-nitrobenzo-2-oxa-1,3-diazolyl)-1 ,4-diazaheptane (Alp-NBD). Sixty to 75% of the staining was specific (displaceable by unlabeled antagonists). Most of the antagonist-occupied beta receptors were immobile, because only 15-25% of their fluorescence recovered on the experimental time scale at 23 degrees C. This immobility correlates with the clustered distribution of Alp-NBD--beta-receptor complexes at 4 degrees C and 37 degrees C. The beta receptors appear to be aggregated prior to antagonist binding, because visible patches were observed immediately after labeling for 30 sec at 4 degrees C. Preincubation at 37 degrees C with (--)-isoproterenol, a beta agonist, prior to Alp-NBD labeling induced a time-dependent release of the beta receptors to a more homogeneous distribution and increased the mobile fraction to 70-80% (lateral diffusion coefficient = 1.4 X 10(-9) cm2/sec at 23 degrees C). This is not due to an effect on membrane fluidity, because the diffusion coefficient of a lipid probe was not altered. The time course of agonist-induced beta-receptor mobilization correlates with receptor loss and adenylate cyclase desensitization but is much slower than adenylate cyclase activation. This indicates that adenylate cyclase activation by beta receptors does not require macroscopic lateral mobility of the majority of the beta receptors.

Adrenergic beta-Antagonists↗
PubMed1981

A fluorescence photobleaching study of vesicular stomatitis virus infected BHK cells. Modulation of G protein mobility by M protein.

The mobility of vesicular stomatitis virus (VSV) G protein on the surface of infected BHK cells was studied by using the technique of fluorescence photobleaching recovery. The fraction of surface G protein that was mobile in that time scale of the measurement (minutes) was at least 75%, a relatively high value among cell surface proteins so far observed. For studies of the effect of an internal viral protein (M protein) on G protein mobility, cells infected with wild-type VSV were compared with those infected with temperature-sensitive VSV mutants of complementation group III, which contains lesions in the M protein. At the permissive temperature, a pronounced decrease in the mobile fraction of surface G was observed for each of three mutants studied, while mobility of surface G at the nonpermissive temperature was indistinguishable in mutant and wild-type infected cells. A significantly lower mobile fraction of G protein was also observed in SV40 transformed 3T3 cells infected with wild-type VSV, but not in 3T3 or chick embryo fibroblast cells similarly infected. None of the variables tested had a measurable effect on the lateral diffusion coefficient of the mobile G protein. These results are interpreted as modulation of the mobility of a specific cell surface protein by a specific intracellular protein.

Animals↗
PubMed1981

Fluorescence photobleaching recovery measurements reveal differences in envelopment of Sindbis and vesicular stomatitis viruses.

Fluorescence photobleaching recovery (FPR) measurements of virus glycoproteins on the surfaces of cells infected with vesicular stomatitis virus (VSV) and Sindbis virus showed that the VSV glycoprotein (G) remained mobile throughout the infectious cycle, whereas Sindbis virus glycoproteins (E1, E2) were partially mobile early after infection and immobile at later times when greater amounts of these proteins were on the cell surface. A highly mobile fraction of Sindbis virus glycoproteins was detected throughout the replication cycle of a temperature-sensitive mutant unable to form virus particles. This immobilization of E1 and E2 was the result of increasing surface glycoprotein concentrations and virus budding. Together with other data, which included the detection of E1 and E2 in particles as soon as these proteins were transported to the cell surface, the FPR results suggest that Sindbis virus assembly initiates on intracellular vesicles, where glycoproteins aggregate and bind nucleocapsids. In contrast, our FPR data on VSV support a model previously suggested by others, in which a small fraction of cell-surface G is immobilized into budding sites formed by interactions with virus matrix and nucleoproteins. FPR measurements also provide direct evidence for strong interactions between E1 and E2, as well as between E1 and PE2, the precursor form of E2.

Animals↗
PubMed1981

Inhibition of the mobility of mouse lymphocyte surface immunoglobulins by locally bound concanavalin A.

Fluorescence photobleaching recovery was used to study directly and quantitatively the inhibition of the lateral mobility of surface immunoglobulins (sIg) on mouse lymphocytes by localized binding of concanavalin A (Con A) coupled to platelets. Up to a threshold occupancy of about 10% of the upper cell surface by Con A-platelets, the diffusion coefficient and mobile fraction of sIg remained as in untreated cells (5.3 X 10(-10) cm2/sec and 0.65, respectively). At higher surface occupancy, these values decreased to 8 X 10(-11) cm2/sec and 0.11. The magnitude of the effect was independent of the percentage occupancy above the threshold and of the distance from the bound Con A-platelets, indicating a cooperative and propagated phenomenon. Treatment with colchicine or cytochalasin B separately induced only partial reversal of the Con A-induced modulation. Treatment with both reversal of the Con A-induced modulation. Treatment with both drugs together was synergistic and fully reversed the mobility inhibition. The modulation was unaffected by NaN3 and 2-deoxyglucose, suggesting no dependence on metabolic energy. Con A-platelets did not affect the mobility of a lipid probe. Models for the Con A-induced modulation and the relationship between the effects of Con A on sIg mobility and patch formation are discussed.

Animals↗
PubMed1980

Fluorescence photobleaching recovery measurements of surface lateral mobilities on normal and SV40-transformed mouse fibroblasts.

Lateral mobilities of fluorescent cell surface probes have been measured on normal (3T3) and transformed (SV3T3) cultured mouse fibroblasts. There is little discernible difference in the mobilities of a lipid analogue (diI), a fluorescent ganglioside derivative (GM1), and tetramethylrhodamine-labeled succinylated concanavalin A. The two cell lines showed expected differences in their abilities to grow in agar, to grow without serum, and to be agglutinated by lectins, indicating that changes of these properties in transformed cells are probably not mediated through increased overall membrane fluidity but are associated with distinct alterations in the mobilities of cell surface receptors. Both fluorescent dextran derivatives and antimouse cell surface antibodies were distinctly less mobile on SV3T3 cells, and the mobile fraction of Con A receptors was lower on SV3T3 cells.

Animals↗
PubMed1980

Lateral diffusion of membrane lipids and proteins during the cell cycle of neuroblastoma cells.

The fluorescence photobleaching recovery method has been used to determine the lateral mobilities of membrane lipids and proteins during the cell cycle of synchronized C1300 mouse neuroblastoma cells (clone Neuro-2A). As probes for lipid mobility, 3,3'-dioctadecylindocarbocyanine iodide and a fluorescein-labeled analog of ganglioside GM1 were used. Membrane proteins were labeled with rhodamine-labeled rabbit antibodies against mouse E14 cells. For both lipid probes the diffusion coefficients reach a minimum in mitosis, increase 2- to 3-fold during G1, remain constant at maximal values during S, and decrease again shortly before mitosis. Membrane proteins also exhibit minimum diffusion coefficients in mitosis, followed by a similar rise in G1. However, as cells proceed through S and G2, the lateral mobility of the membrane proteins gradually decreases. It is argued that lipid mobility is controlled by the fluidity of the membrane lipid matrix whereas protein mobility is governed also by other constraints.

Animals↗
PubMed1979

Lateral diffusion of membrane lipids and proteins is increased specifically in neurites of differentiating neuroblastoma cells.

Lateral diffusion of membrane lipids and proteins was determined in differentiating C1300 mouse neuroblastoma cells by fluorescence photo-bleaching recovery measurements. It is demonstrated that upon differentiation the lateral diffusion of membrane lipids and proteins is increased specifically in the extending neurites. This indicates the appearance of a topographical heterogeneity in the cell membrane, whereby more fluid domains become located in the membrane of the neurites.

Animals↗