Biomedical subjects

L V Gordeeva

Publications and source records attributed to L V Gordeeva.

5 recordsLinked to original sources

PubMed1991

Restoration of adhesive potentials of Ehrlich ascites carcinoma cells by modification of plasma membrane.

A novel technique for modulating the spreading of ascites cells has been developed. Plasma membranes of Ehrlich ascites carcinoma cells were modified in two different ways: 1) biotin residues were covalently coupled to membrane components; 2) biotinylated lipid was introduced into plasma membrane. Adhesion and spreading of modified cells on avidin-coated substrates were studied and compared to those of non-modified cells. Both types of membrane alteration were shown to induce specific (biotin-dependent) interaction with immobilized avidin with resultant cell spreading. Spread cells attained epithelioid-like morphology with the formation of wide thin lamellae, focal contacts with substrate, and circular actin bundles. The process of spreading was shown to be energy-dependent: it could be blocked by metabolic inhibitors and by low temperature. Formation of extended lamellae was prevented by preincubation of cells in the presence of cytochalasin B. The effects of metabolic poisons, low temperature, and microfilament--disruptive drugs were reversible and after the restoration of physiological conditions the cells resumed the spreading process. Immunoprecipitation of biotinylated cell lysates with antiserum to cytoplasmic domain of beta 1-integrin subunit revealed a major 110 kD avidin-binding component. We conclude that lack of spreading of ascites carcinoma cells may be explained by the lack of functionally active adhesion- and spreading-competent cell-surface receptors, but may not be attributed to the defects in intracellular function or organization. Intracellular machinery of cell spreading is preserved in these ascites cells and could be turned on by cell attachment to the substrate via artificial adhesive site incorporated into plasma membrane.

Animals↗

PubMed1989

Lectin-bearing liposomes: differential binding to normal and to transformed mouse fibroblasts.

The binding of covalent conjugates of concanavalin A (Con A) or wheat germ agglutinin (WGA) and liposomes (lectin-liposomes) to the surface of normal and transformed mouse fibroblasts was studied. Quantitation of the binding was performed by means of microfluorometry and radioactive lipid label counting using both sparse and dense cell cultures. It was found that 2.5-3 times more lectin-conjugated liposomes are bound to L or SV3T3 cells than to the mouse embryo fibroblasts and 3T3 cells in a broad concentration range. The binding of Con A- and WGA-liposomes was inhibited up to 70% in the presence of the corresponding carbohydrate inhibitors. A decreased binding of lectin-liposomes to cells was also observed when cells were pretreated with the free lectin. Trypsinization of the cells resulted in an increase in the Con A-liposomes binding to normal fibroblasts. When free fluorescent Con A or WGA was used in binding studies no profound differences in the binding of lectin to normal or transformed cells were detected. The relation of the lectin-liposome/cell to cell/cell interactions is discussed.

Animals↗

PubMed1988

Adhesion defect of ascites cells corrected with membrane-bound attachment molecules.

Adhesion is obligatory for cell proliferation in most types of cells. This function becomes defective after malignant transformation. An extreme example is ascites cells which proliferate in suspension. The nature of their defects remains obscure. Here we show that the linking of biotin molecules to the Ehrlich ascites carcinoma cells enables these cells to spread normally on an avidin-coated substrate. The spreading was the result of specific avidin-biotin interaction. The morphology of the spread cells and sensitivity to different inhibitors are similar to those of normal epithelia. Thus it is enough to supply appropriate substrate-adhesive molecules to the ascites cell surface to normalize their adhesion.

Animals↗

PubMed1986

[Interaction of epithelial cells with the edges of fluid and solid lipid films].

Capping of Concanavalin A (Con A) on the surface of epithelial cells near the cell-cell contacts has been compared with that in the regions of cell contacts with the edges of lipid films. If the lipids are in "fluid" state, Con A is capped likely as on the free edges of epithelial sheets, while contacts with the edge of solid lipid film inhibit capping of Con A as do cell-cell contacts. The same is true for capping of liposomes adsorbed on the surface of epithelial cells. We suppose that solid rather than fluid domains in plasma membranes may play a significant role in establishing cell-cell contacts.

Animals↗

PubMedDate not supplied

[Possibility to study cell membrane topography using tritium planigraphy].

The method of tritium planigraphy was adopted for the investigation of intact cells. Conditions for the incorporation of thermally activated tritium atoms in the erythrocytes are described. The accessibility of erythrocytes hemoglobin for tritium was compared to that of free hemoglobin. By comparing specific radioactivities of amino acids it was shown that the incorporation of the label into free hemoglobin was over 100 times higher than into that in erythrocytes. The cell membrane was highly tritiated. Thus the plasma membrane protects the cell inner regions from penetration of the hot tritium atoms. Tritium planigraphy can be used for studying the cell surface topography.

Amino Acids↗