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At least 37 records · Page 2Linked to original sources
PubMed2000

Stabilization of lysosomal membrane and cell membrane glycoprotein profile by Semecarpus anacardium linn. nut milk extract in experimental hepatocellular carcinoma.

Semecarpus anacardium Linn. nut milk extract administered orally at a dose of 200 mg/kg/day for 14 days exerted an in vivo stabilizing effect on lysosomal membrane and glycoprotein content in rat hepatocellular carcinoma. This was demonstrated in normal rats and in animals whose biomembranes were rendered fragile by induction of hepatocellular carcinoma with aflatoxin B(1) and subsequent treatment with Semecarpus anacardium nut extract. In this condition, the discharge of lysosomal enzymes increased significantly with a subsequent increase in glycoprotein components. The nut extract administration reversed these adverse changes to near normal in treated animals. The possible reason for this reversal is discussed. Such stabilization of biomembranes by Semecarpus anacardium nut extract may have a beneficial effect in the treatment of hepatocellular carcinoma and other cancers involving abnormal fragility of lysosomes and glycoprotein content providing the extract demonstrates safety in a full toxicity study.

Administration, Oral↗
PubMedDate not supplied

Heat-induced alterations in cell membrane permeability and cell inactivation of transformed mouse fibroblasts.

Hyperthermia, has recently been extended in many permutations as a modality of anticancer treatment, but the mechanisms underlying heat-induced cell inactivation are poorly understood. In this study, the role of the cell permeability barrier in the process of heat cytotoxicity are examined. Changes in cell membrane permeability were determined by following the efflux of normally impermeant metabolites, e.g. nucleotides, in cultures of Swiss mouse 3T3 cells, and their transformed derivatives, 3T6 cells. The increase in cell membrane permeability as a function of temperature and exposure duration was found to be characterized by a sigmoid curve, with a threshold value, above which the permeability markedly increased. A correlation was found between cell membrane permeabilization and cell inactivation. Both heat-induced permeabilization and heat cytotoxicity were more pronounced in the transformed cells, as compared to their untransformed counterparts. The temperature-dependent permeabilization was more effective in the presence of the ionophore amphotericin B. The data suggest that heat-induced lesion in the cell membrane has a major role in hyperthermia cytotoxicity.

Amphotericin B↗
PubMed1968

Relation between Epstein-Barr viral and cell membrane immunofluorescence of Burkitt tumor cells. I. Dependence of cell membrane immunofluorescence on presence of EB virus.

A comparison was made of the immunofluorescence tests for detection of cell membrane and Epstein-Barr virus antigens in cells from Burkitt tumor biopsies or continuous cultures derived therefrom. On the whole, cell membrane fluorescence in established lines appeared to depend not only upon the presence of EBV but to a considerable degree also upon the extent of the persistent viral infection. There was no constant relationship, however, between the results of the two tests and exceptions to the rule were noted. These observations indicate that different antigens are involved in the two tests. Biopsy cells in general and young cultures may reveal strong MIF activity but few, if any, EBV-positive cells. The reverse, the presence of relatively large numbers of EBV antigen-containing cells in the absence of significant MIF reactions, was also noted on occasion in a few established cultures. The possible interpretations of these findings have been discussed.

Antigens↗
PubMed1981

Independent control of selected insulin-sensitive cell membrane and intracellular functions-the linkage of cell membrane and intracellular events controlled by insulin. III. The influence of trypsin on cell membrane hexose transport and on glycogen synthase and mitochondrial pyruvate dehydrogenase activation.

Brief treatment of rat adipocytes with low concentration of trypsin activated both cell membrane and intracellular insulin-sensitive functions in marked contrast H2O2 (1), increase in pH, and oxidized glutathione (papers I and II). Glucose oxidation was activated maximally by trypsin in 30 s and preceded maximal activation of glycogen synthase, which occurred in 60s. Trypsin action to activate glycogen synthase was further enhanced by insulin. Mitochondrial pyruvate dehydrogenase was also rapidly activated by trypsin. With both insulin and trypsin action, mediator generation was directly demonstrated by glycogen synthase phosphoprotein phosphatase activation. Trypsin is thus the most insulin-like of these four agents studied since it acts by the formation of chemical mediator peptide(s) which are similar but not identical to those produced by insulin.

Adipose Tissue↗
PubMed1992

Effects of inhibitors and ion substitutions on oscillations of cell membrane potential in cells expressing the RAS oncogene.

Previous studies revealed that in NIH fibroblasts expressing the ras oncogene but not in other NIH fibroblasts, bradykinin leads to sustained, calcium dependent oscillations of cell membrane potential by repetitive activation of calcium-sensitive K+ channels. The present study has been performed to test for ion and inhibitor sensitivity of these oscillations. Both, Lys-bradykinin (kallidin) and bradykinin, but not any shorter peptide tested, maintained the oscillations. The oscillations are abolished in the presence of the K+ channel blocker barium (10 mmol/l). The amplitude but not the frequency of the oscillations is dependent on the extracellular potassium concentration. The oscillations are not dependent on the presence of extracellular sodium, bicarbonate or chloride. The oscillations are abolished in the absence of extracellular calcium and their frequency is significantly decreased at reduced extracellular calcium (to 0.2 mmol/l). The oscillations are not inhibited by acute administration of ouabain (0.1 mmol/l), by dimethylamiloride (100 mumol/l), furosemide (1 mmol/l) and hydrochlorothiazide (100 mumol/l), by cobalt (100 mumol/l), zinc (100 mumol/l), gadolinium (100 mumol/l), verapamil (10 mumol/l) and diltiazem (10 mumol/l), but are abolished in the presence of 100 mumol/l lanthanum, 1 mmol/l cadmium, 10 mumol/l nifedipine, 25 mumol/l SK & F 96365 and 200 mumol/l TMB-8. Stimulation of calcium entry by 10 nmol/l ionomycin is frequently followed by oscillations of cell membrane potential even in the absence of bradykinin. In conclusion, in cells expressing the ras oncogene bradykinin leads to sustained activation of calcium channels at the cell membrane, which cause oscillations of the cell membrane potential by triggering intracellular calcium release.

Animals↗
PubMed1997

A 65-kDa trypsin-sensible membrane cell protein as a possible receptor for dengue virus in cultured neuroblastoma cells.

Dengue virus infects primary neurons in mouse experimental model and tissue culture cells of the central nervous system (CNS). In the present work, a mouse neuroblastoma cell line (N1E-115) and a human neuroblastoma cell line (SK-N-SH), susceptible to dengue virus infection were used to study the presence of cell membrane receptor for dengue-2. By day 5 postinfection (pi), viral antigen was detected by immunofluorescence in the cytoplasm and surrounding the nucleus of N1E-115 cells, while on day 7 pi, it was also present along neural extensions. Infection of N1E-115 cells was diminished with trypsin treatment but not with neuraminidase or endoglycosidase H. Partially purified cell membrane proteins from neuroblastoma cells were analyzed by the Virus Overlay Protein Blot Assay (VOPBA), and a single band migrating at 65 kDa was detected in mouse and human neuroblastoma cells but not in C6, a non-susceptible rat glial cell line which was included as a negative control. The 65 kDa protein was eliminated only when nitrocellulose membranes were treated with trypsin. Analysis of neuronal cell infection by dengue virus provides a useful tool to understand the nature of cellular receptors and mechanisms involved in the infection of the nervous system by dengue viruses.

Animals↗
PubMed1991

Bradykinin-induced oscillations of cell membrane potential in cells expressing the Ha-ras oncogene.

Products of ras genes are putative elements of growth factor signal transduction. However, the mechanism of action of these proteins in normal and malignant growth is as yet obscure. To test for functional consequences of ras oncogene expression, electrophysiological experiments were performed on NIH-3T3 fibroblasts transfected with a transforming Ha-ras MMTV-LTR construct expressing the oncogene on treatment with dexamethasone (+ras). Transfected cells in the absence of dexamethasone (-ras) and nontransfected cells in the presence of dexamethasone (oras) served as controls. In -ras and oras, bradykinin induces a single, transient hyperpolarization. In +ras, bradykinin elicits oscillations of cell membrane potential throughout the presence of the hormone by activation of calcium-sensitive K+ channels. The oscillations of cell membrane potential are abolished in the absence of extracellular calcium. As evident from fura 2 fluorescence, bradykinin leads to a transient increase of intracellular calcium both in the presence and absence of extracellular calcium. Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange. Bradykinin induces oscillations of cell membrane potential similarly in -ras cells loaded with GTP[S], a nonhydrolyzable analogue of GTP. Thus, the altered response of ras oncogene expressing cells to bradykinin relates to the GTP binding property of the ras protein. It is concluded that in cells expressing ras oncogene but not in other fibroblasts bradykinin mimicks the effect of growth factors on the cell membrane.

Bradykinin↗
PubMed1993

The effect of laminin on molecular motion in the cell membrane and on cell motility.

We have studied the variation of lateral diffusion of proteins in the cell membrane, of membrane lipid fluidity and of the electrophoretic motility (EPM) of macrophages after treatment with extrinsic laminin. The results showed that the lateral diffusion coefficient D value of membrane proteins, the fluidity of membrane lipids and the EPM of macrophages were decreased after laminin had bound to its membrane receptor on the macrophages. These results are important for developing an understanding of the early reaction of plasma membranes and cells in the presence of laminin.

Animals↗
PubMed2001

Acute activation of gp130 gene expression in bone marrow stromal cells by contact with myeloma-derived lymphoblastic cell line ARH77 cell membranes.

Cell-cell contact of myeloma-derived cell lines (MDCL) or fresh myeloma cells with bone marrow stromal cells (BMSC) is known to induce interleukin-6 (IL-6) and matrix metalloproteinase-1 (MMP-1) production by a marrow stromal cell line. To determine if other BMSC transcripts are altered during cell-cell contact between BMSC and tumor cells, we have used cell lines ARH77 and U266 in an in vitro model. Using mRNA differential display and reverse transcriptase-polymerase chain reaction (RT-PCR), it was determined that a total of 141 transcripts were either upregulated or downregulated in the BMSC on contact with cell membrane from cell lines ARH77 and U266. Induction of two of these transcripts, interleukin-6 (IL-6) and gp130 in the BMSC by ARH77 cell membranes was studied in greater detail. Real-time PCR was used to quantitate transcript levels of gp130, IL-6, and 36b4, a housekeeping gene. Cycloheximide (CHX) alone increased both gp130 and IL-6 transcripts in the BMSC. In addition, CHX caused a superinduction of these transcripts in BMSC exposed to ARH77 cell membranes. The induction of gp130 was independent of the increase in IL-6 mRNA. Upregulation of gp130, a component of the membrane receptors for the IL-6 superfamily, can have profound effects on the response of BMSC to the IL-6 superfamily of cytokines.

Antigens, CD↗
PubMed1990

How to kill cancer cells: membranes and cell signaling as targets in cancer chemotherapy.

Most approaches to cancer chemotherapy have centered around the idea that cytotoxic drugs can be used to eradicate proliferating neoplastic cells. Cytotoxicity is generally thought to evolve from the presence of drug-induced damage to the genetic material, and DNA has served admirably as a primary focus for drug development. Other cellular targets should also be vulnerable, however, and over the past decade the plasma membrane in particular has received considerable attention as a therapeutic locus. In the early stages of this work there were only vague notions as to how membrane disruption could lead to cell death, but recent thinking has coalesced around the idea that cell-surface signal transduction and growth control pathways represent an ideal target for the rational development of new cancer therapies. In this review, we discuss three aspects of signal transduction-phosphoinositide turnover, phosphorylation by protein kinase C, and phosphorylation by protein tyrosine kinases--and summarize the existing evidence that these vital processes can be specifically disrupted, and that such pharmacology offers rich prospects for future therapeutic design.

Humans↗
PubMed1990

Secretory organelle docking at the cell membrane of Paramecium cells: dedocking and synchronized redocking of trichocysts.

We present the first evidence that secretory organelle docking at the cell membrane can be reversed in vivo. In nondischarge (nd) mutants of Paramecium tetraurelia all trichocysts can be detached from the cell surface within 2-3 h by different means, including cytochalasin B (but not D), high cell density, or Ca2+ ionophores. Considering the well-established ultrastructural differences between nd and wild-type (wt) cells, one can conclude that trichocyst docking at the cell periphery involves two docking sites (I, II): Site I ties the organelles to the epiplasm, and site II is the connection to the cell membrane at the fusogenic zone (expressed only in wt cells); both sites are close to the cell surface and only 150 nm apart. When the trigger for detachment of cortically docked trichocysts (high cell density, cytochalasin B) is relieved, trichocysts are synchronously reattached at the cell membrane, within 40-50 min, with a rate of 20-40 organelles/min, which far exceeds spontaneous docking rates. This is therefore also the first report on synchronization of secretory organelle docking. It is shown by radioactive leucine labeling that the same organelles are redocked, because trichocyst biogenesis is minimal under the conditions of de/redocking used. Surprisingly not only redocking but also detachment of trichocysts from the cell surface can be abolished by inhibitors of protein synthesis. Since Ca2+ ionophores mimic the effects of other conditions sufficient to detach trichocysts from the cell surface, we assume that a protein-dependent mechanism sensitive to Ca2+ (or other ions in exchange) may operate in trichocyst detachment. The precise mechanism involved in attachment or detachment of trichocysts remains to be elucidated.

Animals↗
PubMed1983

Prevention of complement activation on the homologous cell membrane of nucleated cells as well as erythrocytes.

A C3b receptor, a glycoprotein with a molecular weight of 205 kDa (gp205) on human erythrocytes (Ehu), has been claimed to restrict the activation of human complement via the alternative complement pathway (ACP), thereby inhibiting the activation of the ACP even on neuraminidase (Nase)-treated Ehu. However, the Nase-treated Ehu were sensitive to hemolysis by guinea pig complement via ACP activation, although the C3b receptors on Ehu can react with guinea pig C3b. Furthermore, HeLa cells which had no detectable C3b receptor did not became reactive with guinea pig ACP. On the contrary, Nase treatment of guinea pig erythrocytes (Egp) as well as guinea pig line 10 tumor cells, which have no detectable C3b receptor, could not make those cells reactive with the homologous guinea pig ACP although they became reactive with human and rabbit ACP. Similarly, rabbit E did not become reactive with the homologous rabbit ACP following Nase treatment. Nase-treated Egp preincubated with human serum in the presence of EDTA were also not lysed by guinea pig serum. Therefore the unreactiveness of Nase-treated cell membrane with homologous ACP was not merely due to the absence of antibody to cell membrane in the homologous serum. There may be a membrane inhibitor which preferentially interacts with homologous complement to circumvent undesirable complement activation on the homologous cell membrane.

Animals↗
PubMed1984

Lipid analyses and fluidity studies by electron spin resonance of red cell membranes in hereditary high red cell membrane phosphatidylcholine hemolytic anemia.

Membrane lipid analyses and electron spin resonance (ESR) studies of membrane fluidity were carried out on the red cells of a Japanese patient with hereditary high red cell membrane phosphatidylcholine hemolytic anemia (HPCHA). Increased amounts of phosphatidylcholine (PC) and cholesterol were found in the membrane lipids of the affected patient, despite normal plasma lipids. The order parameter of cholesterol-free pure phospholipid liposomes prepared from this patient's red cells was decreased, apparently because of the increased PC. In contrast, the order parameter of the total red cell lipid liposomes (containing free cholesterol) was essentially normal. The overall fluidity of the intact red cells was determined by ESR with a spin probe, 5-SAL. Again, the order parameters were normal in the intact red cells of the patient with HPCHA. This suggests that the concomitant increase of membrane cholesterol and phosphatidylcholine serves to maintain normal membrane fluidity in the HPCHA red cells.

Aged↗
PubMed1989

1-anilino-8-naphthalenesulphonate binding parameters in red cell membranes. Does diabetes mellitus affect cell membrane dynamics?

In this study we report the use of 1-anilino-8-naphthalenesulphonate as a fluorescence probe to investigate the properties of plasma membranes derived from normal and diabetic red blood cells. The binding of 1-anilino-8-naphthalenesulphonate to diabetes-affected erythrocyte membranes, as compared with controls, was measured by means of fluorescence polarization and fluorescence titration techniques. These measurements demonstrated anomalous 1-anilino-8-naphthalenesulphonate binding to pathological red cell membranes. The amount of 1-anilino-8-naphthalenesulphonate bound to diabetic erythrocyte membranes was greater than that of controls. This fluorometric study indicated that the outer monolayer binding of 1-anilino-8-naphthalenesulphonate was markedly augmented in the erythrocyte membranes of diabetic patients. Significant correlations were found between 1-anilino-8-naphthalenesulphonate binding parameters and membrane lipid composition. The correlation between these binding parameters and non-enzymatic protein glycation was poor or moderate. Though the fluorescence intensity and emission maximum were quite similar in both groups investigated, binding studies revealed that there were approximately 1.2 times the number of 1-anilino-8-naphthalenesulphonate binding sites and a 33% increase in the KD value in diabetic membranes, suggesting significant differences in the environment of the 1-anilino-8-naphthalenesulphonate binding sites in these two groups of patients. The results presented in this report indicate that (a) 1-anilino-8-naphthalenesulphonate is a sensitive probe of membrane architecture alterations, and can be used to elucidate the perturbating effects of sterols in membrane systems, and (b) that significant differences in membrane dynamics exist between normal and diabetic red cell membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗