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At least 19 recordsLinked to original sources
PubMed1993

Characterization of monocyte-activating tumour cell membrane structures.

Tumor cells are known to activate monocytes/macrophages and it has been shown that this stimulation was conferred by tumour-cell membranes. In order to analyse the relevant structures for tumor cell-specific TNF-induction monocytes from healthy donors were cultured in the presence of plasma membrane preparations from Jurkat or K562 cells. Both tumour cell lines revealed a monocyte-stimulating plasma membrane component of about 45 kDa. The TNF-inducing factor exhibited characteristics of a glycoprotein with the carbohydrate moiety as the structure responsible for stimulation. CD2, a glycosylated T-cell specific membrane component, was identified as being involved in monocyte activation in the case of the Jurkat cells whereas the identity of the activating structure on K562 cells is still unknown. From the data presented here indicating the importance of carbohydrate structures for monocyte activation we conclude that altered glycosylation of cell surface molecules of tumour cells might be responsible for tumour cell-induced monocyte stimulation.

Antigens, Differentiation, T-Lymphocyte↗
PubMedDate not supplied

[Cell membrane structures participating in mast cell-lymphocyte interactions].

Membrane structures of the mast cells are mainly of protein nature, since trypsin treatment causes almost complete loss of mast cell ability to form rosettes. Trypsin-sensitive proteins have no critical role in the formation of membrane thymocytes structures, which cause their affinity to the mast cells. Sialic acids play a role in organization of the membrane thymocyte structures.

Animals↗
PubMed1978

Cell membrane structure of human giant-celled glioblastoma.

A giant-cell glioblastoma was examined by electron microscopy and by the freeze-fracture technique. The cell membranes bordering the extensive extracellular space often showed complicated undulations and peripheral vacuoles as well as occasional microvilli or filopodia. The undulations were mainly composed of plasmalemmal vesicles as well as of large (400--800 nm in diameter) and small (30--50 nm in diameter) localized protrusions and invaginations of the cell membrane. Deep invaginations of the cell membrane apparently resulted in two separate cytoplasmic portions. Locking of protruded cytoplasmic tongues and adherens junctions were sometimes seen in closely approximated cell membranes. The average number of membrane particles per micrometer2 was 630 +/- 130 on the P face and 180 +/- 30 on the E face. The membrane particles were occasionally aggregated to form clusters about 30 to 150 micrometer in diameter. Gap junctions were occasionally found, but there were no tight junctions. Large particles about 30 nm in diameter were found in places.

Cell Membrane↗
PubMedDate not supplied

Do changes in the cell membrane structure induce the generation of lipid peroxidation products which serve as first signalling molecules in cell to cell communication?

Evidence is presented that mammalian and plant cells respond equally to any event which changes their cell membrane structure. Proliferation, wounding or aging induces generation of lipidhydroperoxides from cell wall phospholipids. These are transformed to signalling compounds, some of these induce apoptosis. If the exerted impact exceeds a certain level, the original enzymic reaction switches to a non-enzymic one which produces peroxylradicals. The latter are not liberated enzymically. Peroxylradicals generate a second set of signalling compounds, but cause also severe damage: they epoxidize double bonds, and oxidize proteins, sugars and nucleic acids. Such reactions occur in all inflammatory diseases. Lipidhydoperoxides and their degradation products are incorporated in fat. Apparently, these compounds are transferred partly to LDL. Such LDL is still recognized by the cell LDL receptor. Toxic lipid peroxidation products are therefore introduced into cells and might be able to damage cells from inside long before the typical signs of atherosclerosis and other chronic diseases become visible.

Animals↗
PubMed1975

Electrophoresis of lymphoid cells. Differences in the cell membrane structure of murine thymocytes, T and B cells revealed by enzyme and formalin treatment.

Low concentrations of protease and trypsin reduced the electrophoretic mobility (EPM) of thymocytes; with higher concentrations it was normal or above. Differences in membrane structure of thymocytes, T and B cells was found as B cells showed no reduction while T cells gave intermediate values. Further the reduction was greater with protease than with trypsin. Formalin fixation increased the EPM of all normal cell types to a similar degree. The EPM of proteolytically treated thymocytes and B cells was increased to a similar level and to a greater degree than neuraminidase-treated thymocytes. Small amounts of sialic acid were detected in the supernatant after proteolytic treatment of thymocytes. Protease reduced the binding of anti-lymphocyte serum, while no definite effect was obtained with trypsin. Neither sublytic doses of phospholipase C nor ribonuclease appeared to change the EPM.

Animals↗
PubMed1984

F-Met-Leu-Phe and echo 9 virus interaction with human granulocytes. Changes of cell membrane structure.

Biophysical and biochemical methods were applied for investigation of cell membrane properties of human polymorphonuclear leukocytes (PMNs) exposed to the chemotactic peptide N-formylmethionyl-leucylphenylalanine (f-Met-Leu-Phe) and echovirus type 9, strain A, Barty. Steady-state fluorescence depolarization with diphenylhexatriene demonstrated no gross changes of the total membrane fluidity under the different experimental conditions. However, by means of the monomer-excimer technique with pyrenedecanoic acid (PDA), significant changes of the local membrane structure were detected for both agents. As demonstrated by a higher excimer ratio, the membrane area available for the PDA molecules was restricted by f-Met-Leu-Phe. This effect was dependent on the dose and on the time of interaction of the chemotactic peptide. These experimental findings were explained by the formation of functional receptor units ("activated membrane"). Echo 9 virus exhibited the opposite effect, characterized by a higher ratio of monomers, which also depended on the viral dose and the time of virus-PMN interaction. These virus-induced findings were explained by the dissolution of functional receptor units. Consecutive exposure of the PMNs to f-Met-Leu-Phe and echovirus, or vice versa, demonstrated a virus-predominant effect on the membrane structures.

Cell Membrane↗
PubMed2002

Are changes of the cell membrane structure causally involved in the aging process?

Lipid peroxidation is recognized by proliferation, wounding, and aging. The connecting link between these different events is a change in cell wall structure, which activates membrane bound phospholipases. These cleave phospholipids. Thus liberated polyunsaturated fatty acids (PUFAs) are substrates for lipoxygenases, which accept equally well linoleic acid and arachidonic acid and generate lipid hydroperoxides (LOOHs). If the amount of free PUFAs exceeds a certain amount, lipoxygenases commit suicide. The consequence is liberation of free iron ions that react with LOOHs by formation of radicals. These start a chain reaction. LOO* radicals produced in the course of this process attack proteins, nucleic acids, and also double bonds of all unsaturated compounds by epoxidation. Morever LOOHs are decomposed to toxic epoxy acids and alphabetagammadelta-unsaturated aldehydes. Both species react with glutathione. The resulting products seem to induce apoptosis. Since the products generated by wounding or aging are formed by decomposition of LOOHs the investigation of the aging processes can be simplified by studying the physiological action of artificially generated lipid peroxidation products derived from pure PUFAs. Degradation products of LOOHs are generated by thermal decomposition of fat-containing PUFAs. These products are induced into the body by adsorption in the intestine. They are at least partly incorporated in low density lipoproteins (LDLs). Primarily investigations seem to indicate that an overload of a diet rich in PUFAs induces only after two days an increase in oxidized LDL/PUFAs for a factor up to two in young people and for a factor of more than two in old individuals.

Aging↗
PubMed1977

Cell membrane structure of vascular smooth muscle of circle of Willis.

Cell membranes of vascular smooth muscles of the circle of Willis were studied in thin sections and freeze-replicas. The cell membranes were differentiated into a caveolae intracellulares zone and caveolae-free zone, both of which were generally arranged in an alternate manner and parallel to the major axis of the smooth muscle cell. In the former zone, the caveolae intracellulares, about 600 A in diameter, were neatly oriented in one to several rows running parallel to the longitudinal axis of the muscle cell with a center-to center distance of about 800 A. The latter zone was of variable width and smooth, apart from membrane particles or scattered caveolae, and corresponded mainly to the dense area and partially to the myofibril area beneath the cell membrane. Membrane particles were generally more numerous on face A than on face B, and their average number per micronm2 was about twice as many inside the rows of the caveolae as outside. Rosette formations of membrane particles were often evident at the stomal rims of the caveolae. Adherentes and gap junctins were occasionally found on the caveolae-free areas which often protruded externally. Tight junctions appeared as a collection of scattered strands, which frequently showed free ends and were parallel to each other and also to the major axis of the smooth muscle cell.

Animals↗
PubMed1973

A role for anionic sites in epithelial architecture. Effects of cationic polymers on cell membrane structure.

The effects of several cationic polymers (poly-L-lysines, protamine, and histone) on rabbit gall bladder epithelial cells were studied to explore possible roles for negative sites in the membrane. The tissue was bathed for 30 min at 37 degrees C in Ringer's solutions containing from 0.1 to 100.0 microg/ml of cationic polymers, and subsequently was fixed with 1% OsO(4) and examined with the electron microscope. All cationic polymers, at appropriate concentrations, produced similar changes in membrane structure. Adjacent membranes frequently were fused. Membrane structures such as microvilli lost rigidity. Cell membranes showed an apparent increase in permeability as judged by osmotically traumatized cells. These results indicate that fixed anionic sites play significant roles in stabilizing epithelial membrane structures.

Animals↗
PubMed1997

Changes in red blood cell membrane structure in patients with chronic renal failure.

The properties of red blood cell membranes in patients with chronic renal failure were investigated using electron paramagnetic resonance spectroscopy. Using spin traps, 5,5-dimethylpirroline-1 oxide and N-tert-butyl-alpha-phenylnitrone, we found generation of hydroxyl radicals in the blood of patients with chronic renal failure after 20 min of regular hemodialysis. The physical state of membrane proteins and membrane osmotic fragility and reductive properties of red blood cells were studied. The increase in the relative correlation time of 4-(2-iodoacetamido)-2,2,6,6-tetramethylpiperidine-1 oxyl indicates the immobilization of membrane protein molecules in erythrocytes of chronic renal failure patients. The decrease in membrane protein mobility was observed in whole blood incubated with tert-butylhydroperoxide, regardless of the presence of iron. We found that the addition of ferrous ions did not aggravate profound changes in membrane proteins induced with tert-butylhydroperoxide. We also demonstrated higher osmotic fragility of erythrocytes in the patients with renal failure as compared to normal subjects. These alterations in membrane structure of red blood cells in hemodialysed patients suggest that hydroxyl radicals generated during hemodialysis can play an important role in the oxidative mechanism of erythrocyte damage.

Electron Spin Resonance Spectroscopy↗
PubMed1975

Modification of red cell membrane structure by cholesterol-rich lipid dispersions. A model for the primary spur cell defect.

Cholesterol-rich membranes are the hallmark of "spur" red cells. Spur cells accumulate cholesterol from cholesterol-rich serum lipoproteins. Previous studies suggested that this added cholesterol is responsible for both the altered morphology and the destruction of spur cells. To examine this process in the absence of other serum factors, cholesterol-lecithin dispersions with varying amounts of unesterified cholesterol (C) relative to phospholipid (P) were prepared, and their influence on normal human red cells was studied. Cholesterol-rich lipid dispersions (C/P mole ration greater 1.0) transferred cholesterol to both red cell membranes and serum lipoproteins, and cholesterol-poor dispersions (C/P mole ration less 1.0) depleted red cells of cholesterol. Changes in membrane cholesterol paralleled changes in membrane surface area, as calculated from osmotic fragility, with a 0.22 percent variation in surface area per 1.0 percent variation in cholesterol content. Cold-induced compression of membrane surface area was increased in cholesterol-poor red cells (C/P equals 0.4), whereas the surface area of cholesterol-rich membranes (C/P equals 1.80) underwent no compression. Although the Na and K permeability of red cells severely depleted of cholesterol was increased, lesser degrees of depletion had no effect, and the permeability of cholesterol-rich cells was normal. However, increasing membrane cholesterol caused a progressive decrease in red cell deformability, as measured by filtration. Cholesterol-poor red cells were spherocytic in appearance and cholesterol-rich cells were broad and flat, indicative of their surface areas. In addition, cholesterol-rich cells had an irregular contour due to folding of the periphery of the cell. This shape abnormality was identical to that of both spur cells after splenectomy and normal red cells incubated in spur serum. Normalization of the C/P of spur serum by added phospholipid prevented the increase in membrane cholesterol and surface area and the transformation of cell shape. These studies establish that the cholesterol content of red cells is dependent on the C/P of their milieu, either lipoproteins or cholesterol-lecithin dispersions. Moreover, the surface area, deformability, and contour of cholesterol-rich red cells are a direct function of their increased membrane C/P. Although cholesterol-rich spur cells are further modified in the circulation of patients with spleens, this abnormality of the membrane lipid bilayer, induced by cholesterol-rich cholesterol-lecithin dispersions, represents the primary spur cell defect.

Anemia, Hemolytic↗
PubMed1978

Sheep red blood cell membrane structure: an immunological probe.

Pronase digested sheep red blood cell stromata were employed as probe in order to investigate erythrocyte membrane arrangement by immunological way. Antiserum from rabbits immunized with erythrocyte ghost pronase residue assayed for its hemolytic activity against intact sheep red cells, showed an high titer, in a good agreement with the presence in the same residue of externally located membrane antigens. Immunoelectrophoretic analysis was performed between the solubilized residue and precipitins produced by rabbits immunized respectively with the following antigens: intact sheep red blood cells (SRBC), sheep erythrocyte stromata (SRBCS), lipid complex (LC), sphingomyelin complex (SF), stromata after phospholipase A treatment (SPLA), stromata after phospholipase C treatment (SPLC), stromata after phospholipases A and C treatment (SPLAC), and pronase treated stromata (SP). Antigen/antibody reaction with anti-SP antiserum showed an additional precipitation line: this fact is discussed in view of a possible enrichment of the fraction after pronase stromata digestion, and/or enhancement of the immunogenicity.

Animals↗