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At least 199 records · Page 11Linked to original sources
PubMed1982

Cell morphology, cell filaments and cell death during in vitro ageing: aphidicolin and serum deprivation effects on mouse diploid fibroblasts (a correlated scanning electron microscope and immunocytochemical study).

Terminal fibroblasts differ from early ones by slowing down in replicative activity, increase in cell area, changes in the cytoskeleton and changes in the way of dying. Replication was inhibited in early fibroblasts either with aphidicolin or by serum deprivation. Both treatments induce cell flattening and increase in cell surface. Aphidicolin has no effect on actin-microfilaments whereas serum deprivation induces the terminal pattern of filaments in many early cells. After both treatments, fibroblasts keep dying as early cells do. We conclude that there is no direct relation between changes in the organization of cell filaments and slowing down of replication (inducing cell flattening); we suggest that they depend on changes in the cell membrane structure appearing during in vitro terminal differentiation.

Animals↗
PubMed2005

Expression of NADPH oxidase isoform 1 (Nox1) in human placenta: involvement in preeclampsia.

Increased oxidative stress in the placenta has been associated with preeclampsia (PE), a clinical syndrome involving placental pathology. The enzymatic sources of reactive oxygen species in the human placenta are as yet unidentified. We hypothesized that NADPH oxidase is a main source of reactive oxygen species in the placenta and its expression may change in PE. Employing RT-PCR, we have amplified a novel NADPH oxidase isoform Nox1 from human choriocarcinoma BeWo cells. Using polyclonal anti-peptide antiserum recognizing unique Nox1 peptide sequences, we identified by immunohistochemistry and cell fractionation that Nox1 protein localizes in the BeWo cell membrane structures. Immunohistochemistry of normal placental tissues showed that Nox1 was localized in syncytiotrophoblasts, in villous vascular endothelium, and in some stromal cells. At the immunohistochemical level Nox1 expression was significantly increased in syncytiotrophoblast and endothelial cells in placentas from patients with preeclampsia as compared to gestational age-matched controls. Western blot analysis of whole placental homogenate confirmed this increase. Our data suggests that increased Nox1 expression is associated with the increased oxidative stress found in these placentas.

Cell Line, Tumor↗
PubMed2006

PV-1 labels trans-cellular openings in mouse endothelial cells and is negatively regulated by VEGF.

The PV-1 protein is endogenously expressed from a single mRNA in the mouse pancreatic MS-1 endothelial cell line as a 60-kDa N-glycosylated and 50-kDa non-glycosylated protein that form DTT sensitive oligomers. In the absence of cell permeabilization, PV-1 antibodies label transcellular openings of variable size, many that penetrate through the cytosol with circular openings on the free and attached surface of the plasma membrane. Intracellular PV-1 is localized in perinuclear aggregates that can extend as a fibrous network through the cytosol and often surround the nuclear compartment. In some cells, PV-1 is organized as a large unipolar spindle-like structure that is often associated with severe deformation of the nucleus. The VEGF-R2 inhibitor SU5614 increased the PV-1 protein levels in a dose-dependent manner and inhibited MS-1 cell growth, without inducing apoptosis. This report provides compelling evidence for a functional role of PV-1 in the formation of large transendothelial channels and modulation of nuclear shape. Moreover, these data suggest the PV-1 protein is negatively regulated by VEGF.

Animals↗
PubMed2006

Embryonic stem cell-derived microvesicles reprogram hematopoietic progenitors: evidence for horizontal transfer of mRNA and protein delivery.

Membrane-derived vesicles (MV) are released from the surface of activated eucaryotic cells and exert pleiotropic effects on surrounding cells. Since the maintenance of pluripotency and undifferentiated propagation of embryonic stem (ES) cells in vitro requires tight cell to cell contacts and effective intercellular signaling, we hypothesize that MV derived from ES cells (ES-MV) express stem cell-specific molecules that may also support self-renewal and expansion of adult stem cells. To address this hypothesis, we employed expansion of hematopoietic progenitor cells (HPC) as a model. We found that ES-MV (10 microg/ml) isolated from murine ES cells (ES-D3) in serum-free cultures significantly (i) enhanced survival and improved expansion of murine HPC, (ii) upregulated the expression of early pluripotent (Oct-4, Nanog and Rex-1) and early hematopoietic stem cells (Scl, HoxB4 and GATA 2) markers in these cells, and (iii) induced phosphorylation of MAPK p42/44 and serine-threonine kinase AKT. Furthermore, molecular analysis revealed that ES-MV express Wnt-3 protein and are selectively highly enriched in mRNA for several pluripotent transcription factors as compared to parental ES cells. More important, this mRNA could be delivered by ES-MV to target cells and translated into the corresponding proteins. The biological effects of ES-MV were inhibited after heat inactivation or pretreatment with RNAse, indicating a major involvement of protein and mRNA components of ES-MV in the observed phenomena. We postulate that ES-MV may efficiently expand HPC by stimulating them with ES-MV expressed ligands (e.g., Wnt-3) as well as increase their pluripotency after horizontal transfer of ES-derived mRNA.

Animals↗
PubMed1982

A novel effect of salmon calcitonin on in vitro Ca-uptake by rat brain hypothalamus: the regional and hormonal specificities.

It was found that salmon calcitonin-I (sCT) inhibited in vitro 45Ca2+-uptake by rat brain hypothalamus blocks in a dose-dependent manner. The minimum effective concentration was estimated to be 10 nM or less. The effect appeared to be specific to the hypothalamus and was not observed with the pons plus medulla oblongata or the cerebral cortex. Two C-terminal fragments of the fish hormone, sCT (10-32) and sCT (22-32), and porcine calcitonin failed to inhibit the ion-uptake though tested in concentrations abolishing 125I-sCT binding to these brain tissues, indicating that the whole structure of sCT is essential for the inhibitory effect but not for the binding. Another finding to be noted was a possible dependency of this effect on the integrity of the cell membrane structure. A crude synaptosomal fraction subsequently prepared from sCT-exposed hypothalamus blocks exhibited a decreased uptake of 45Ca2+, while a corresponding fraction from unexposed tissue did not respond to the hormone. These characteristics of this novel in vitro effect of sCT suggest its possible relevancy to the anorectic effect which also appears to be specific to the fish hormone.

Animals↗
PubMed2004

[Cardiometabolic therapy of ischemic heart disease].

A total of 59 patients suffering from ischemic heart disease with effort angina (functional classes II-IV) entered the study. Of them, 29 patients received antianginal drugs and 10-day courses of a combination of drugs with membran-oprotective properties (MPD); 30 patients received antianginal drugs alone. Blood levels of lipid peroxidation products, lipid structure of erythrocytic membrane, exercise tolerance were studied before and after the treatment. MPD therapy was associated with lower activity of lipid peroxidation, stabilization of cell membrane structure and greater exercise tolerance due to more effective cardiac performance.

Angina Pectoris↗
PubMed1990

[Concanavalin A binding sites on the cell membrane and other membrane structures of alveolar macrophages].

Concanavalin-A points of linkage were positively detected on cell membranes of alveolar and peritoneal macrophages by means of Con-A ferritin conjugate. Quantitative conclusions were drawn from these findings with regard to the number of mannose and glucose residues per 1 micron 2 of membrane area. With different incubation periods, 15, 25, and 45 minutes, various distribution patterns of ferritin molecules were recorded. They were diffusely distributed in cytoplasma as well as on the outer nuclear membrane. Ferritin particles were identified also on vacuolar membranes and in direct contact with lysosomes.

Animals↗
PubMed1985

Changes in glycosphingolipid composition during differentiation of human leukemic granulocytes in chronic myelogenous leukemia compared with in vitro granulocytic differentiation of human promyelocytic leukemia cell line HL-60.

Changes in glycosphingolipid (GSL) composition during differentiation of human leukemic granulocytes were investigated qualitatively and quantitatively in immature and mature granulocytic cells derived from human chronic myelogenous leukemia (CML) cases and were compared with those found in the in vitro granulocytic differentiation of the human promyelocytic leukemia HL-60 cell line. Two neutral GSLs, ceramide monohexoside and ceramide dihexoside, and two molecular species of gangliosides, one being the ganglio-series ganglioside NeuAc(alpha 2-3)Gal(beta 1-4)Glc-Cer (GM3) and the other being the lacto-series sialosylparagloboside, were predominant in the granulocytic cells at an early maturation stage. During the granulocytic differentiation of CML cells, the contents of ceramide dihexoside and paragloboside increased strikingly with a concomitant decrease in ceramide monohexoside, and the total amount of neutral GSLs increased to about three times as much as that of the most immature granulocytic cells, myeloblasts. On the other hand, lacto-series gangliosides, with longer sugar moieties increased with a concomitant decrease in ganglio-series ganglioside GM3, and the ganglioside profile became more complex. The total content of ganglioside increased in parallel with the complexity of the ganglioside profile. Similar differentiation-associated changes were also found in GSL composition during the in vitro granulocytic differentiation of HL-60 cells. However, a marked difference between the differentiation-dependent change in the GSL composition of CML cells and that of HL-60 cells was observed for a ganglioside species which was found to be one of the major gangliosides in normal neutrophils: in the former, the ganglioside level increased up to the level in normal mature granulocytes as the cells differentiated; in contrast, it decreased significantly during granulocytic differentiation of the latter cells. When the GSL composition of the neutrophils obtained from CML cells, which were apparently normal as to morphology, stimulus-induced membrane potential changes, and superoxide-producing capacity, was compared with that of normal neutrophils, an obvious difference was observed between them, especially with regard to ganglioside GM3; the amount of ganglioside GM3 in the former was about one-sixth of that in the latter. This finding indicates some alterations in the cell membrane structure of neutrophils of CML origin.

Carbohydrate Metabolism↗
PubMed2006

Apical targeting of syntaxin 3 is essential for epithelial cell polarity.

In polarized epithelial cells, syntaxin 3 localizes to the apical plasma membrane and is involved in membrane fusion of apical trafficking pathways. We show that syntaxin 3 contains a necessary and sufficient apical targeting signal centered around a conserved FMDE motif. Mutation of any of three critical residues within this motif leads to loss of specific apical targeting. Modeling based on the known structure of syntaxin 1 revealed that these residues are exposed on the surface of a three-helix bundle. Syntaxin 3 targeting does not require binding to Munc18b. Instead, syntaxin 3 recruits Munc18b to the plasma membrane. Expression of mislocalized mutant syntaxin 3 in Madin-Darby canine kidney cells leads to basolateral mistargeting of apical membrane proteins, disturbance of tight junction formation, and loss of ability to form an organized polarized epithelium. These results indicate that SNARE proteins contribute to the overall specificity of membrane trafficking in vivo, and that the polarity of syntaxin 3 is essential for epithelial cell polarization.

Amino Acid Motifs↗
PubMed1986

Effects of ketoconazole on sterol biosynthesis by Leishmania mexicana mexicana amastigotes in murine macrophage tumor cells.

Murine macrophage tumor cells infected with Leishmania mexicana mexicana were exposed to the antimycotic drug ketoconazole and to [2-14C]mevalonate, then the amastigotes were isolated, collected, purified, and their free sterols were analyzed by chromatographic and mass spectrometric methods. Control amastigotes contained as products of de novo biosynthesis C28 4-desmethyl sterols (episterol, 5-dehydroepisterol), C29 4-desmethyl sterols (stigmasta-7,24 (28)-dien-3 beta-ol, stigmasta-5,7,24(28)-trien-3 beta-ol), 4-methyl sterols (4 alpha, 14 alpha-dimethylzymosterol, obtusifoliol) and a 4,4-dimethyl sterol (lanosterol). Present also were macrophage sterols (cholesterol, desmosterol) and a putative product of the C-24 alkylation of desmosterol by amastigotes (24-methylenecholesterol). Amastigotes from macrophages exposed to ketoconazole showed notable changes in the proportions, concentrations and specific activities of their free sterols; increased for 4 alpha, 14 alpha-dimethylzymosterol and decreased for the endogenous C28 and C29 4-desmethyl sterols. Such changes were observed at a ketoconazole concentration as low as 0.01 microgram ml-1. By contrast, uninfected macrophages accumulated only small amounts of lanosterol of high specific activity at a ketoconazole concentration of 10 micrograms ml-1. the ketoconazole-induced alterations in amastigote sterols parallel those previously reported in fungi and L. m. mexicana promastigotes, and suggest a biochemical mechanism for the anti-leishmanial activity of the drug in which changes in sterol composition are linked to disturbances of cell membrane structure and function, and hence to cytotoxicity.

Animals↗
PubMed1980

Characteristics of fibrous protein and the disulphide cross-linking bond in human stratum corneum.

Fibrous proteins of human stratum corneum were isolated with urea-Tris buffer (pH 9.0) with and without 2-mercaptoethanol (2ME). Comparative studies were made of the biochemical and morphological properties of purified samples obtained with and without 2ME. The final yield of fibrous protein extracted with 2ME was 17 times higher than the yield extracted without 2ME. Identical results were found for the 2 samples by electron microscopic observation, SDS gel electrophoresis with urea and 2ME, and amino acid analysis. However, high molecular weight staining patterns appeared on the SDS gel when the fibrous protein extracted without 2ME was treated with sample buffer containing 4 M urea but no 2ME. These staining patterns were indicative of cross-linking with disulphide bonds. Extraction of the structural proteins with or without 2ME produced the same amount of polymerized fibrous protein. These results suggested that the structural polypeptides of fibrous protein were constructed through ionic forces rather than disulphide bonds. Electron microscopic observation also did not show any differences in the fibrous structures constructed with or without 2ME. The structural polypeptide molecules, than, may be stabilized by partial cross-linking with disulphide bonds. It is possible that the addition of 2ME cleaves disulphide bonds in cell membrane structures and releases fibrous components more effectively than the addition of agents which physically disrupt membrane structures. Consequently, the increase of yield of fibrous protein by the addition of 2ME might be mainly due to cleaving of the membrane structures and partially due to cleaving interpolypeptide disulphide bonds.

Amino Acids↗
PubMed1999

Pharmaceutical therapies for sealing of permeabilized cell membranes in electrical injuries.

Several years ago, we proposed that loss of cell membrane structural integrity by electroporation is a substantial cause of tissue necrosis in victims of electrical trauma. Specifically, this involves the permeabilization of the lipid bilayer by thermal and electrical forces. We further suggested that certain mild surfactants in low concentration could induce sealing of permeabilized lipid bilayers and salvage of cells that had not been extensively heat-damaged. Successful restoration of membrane transport properties using the surfactant poloxamer 188 was reported in 1992. The purpose of this study is to further examine the response of electroporated rat skeletal muscle membranes to poloxamer 188 (P188) therapy by direct assay of membrane transport properties. Experimental evidence accumulated to date suggests that P188 is effective in sealing permeabilized cell membranes both in vitro and in vivo.

Animals↗
PubMed1984

Role of carbohydrates in rat leukemia cell-liver macrophage cell contacts.

The mechanism by which macrophages recognize tumor cells is still unknown. We have studied interactions between rat liver macrophages and rat L 5222 leukemia cells. These tumor cells, but not normal leukocytes or erythrocytes, adhere to freshly isolated macrophages in vitro. Binding of tumor cells by macrophages can be inhibited by N-acetyl-D-galactosamine, D-galactose and more potently by glycoproteins with terminal N-acetyl-D-galactosamine or D-galactose residues. Tumor cell adhesion is calcium-dependent. The relevant leukemia cell membrane structures which bear terminal beta-D-galactosyl or related residues have been determined as trypsin- and pronase-sensitive, and hence may presumably be glycoproteins. The tumor cell receptor on liver macrophages appears to be a lectin with the carbohydrate specificity N-acetyl-D-galactosamine greater than D-galactose greater than L-fucose.

Acetylgalactosamine↗
PubMed1997

Prevention of cardiac arrhythmia by dietary (n-3) polyunsaturated fatty acids and their mechanism of action.

The role of marine fish oil (n-3) polyunsaturated fatty acids in the prevention of fatal ventricular arrhythmia has been established in experimental animals. Prevention of arrhythmias arising at the onset of ischemia and reperfusion is important because if untreated, they result in sudden cardiac death. Animals supplemented with fish oils in their diet developed little or no ventricular fibrillation after ischemia was induced. Similar effects have also been observed in cultured neonatal cardiomyocytes. Several mechanisms have been proposed and studied to explain the antiarrhythmic effects of fish oil polyunsaturated fatty acids, but to date, no definite mechanism has been validated. The sequence of action of these mechanisms and whether more than one mechanism is involved is also not clear. Some of the mechanisms suggested to explain the antiarrhythmic action of fish oils include the incorporation and modification of cell membrane structure by (n-3) polyunsaturated fatty acids, their direct effect on calcium channels and cardiomyocytes and their role in eicosanoid metabolism. Other mechanisms that are currently being investigated include the role of (n-3) polyunsaturated fatty acids in cell signalling mediated through phosphoinositides and their effect on various enzymes and receptors. This article reviews these mechanisms and the antiarrhythmic studies using (n-3) polyunsaturated fatty acids.

Animals↗
PubMed1996

Cytoskeletal changes in podocytes associated with foot process effacement in Masugi nephritis.

Foot process effacement represents the most characteristic change in podocyte phenotype under a great variety of experimental as well as human glomerulopathies. It consists in simplification up to a total disappearance of an interdigitating foot process pattern. Finally, podocytes affix to the glomerular basement membrane by outspread epithelial sheets. Structural and immunocytochemical techniques were applied to analyze the cytoskeletal changes associated with foot process effacement in Masugi nephritis. Three days after injection of the anti-glomerular-basement-membrane serum an interdigitating foot process pattern was almost fully lost; more than 90 percent of the outer glomerular capillary surface were covered by expanded sheets of podocyte epithelium that contain a highly organized cytoskeleton adhering to the basal cell membrane. Structurally, this cytoskeleton consists of an interwoven network of microfilaments with regularly distributed dense bodies, which obviously serve as cross-linkers within this network. Immunocytochemically, the expression of actin, alpha-actinin, and pp44 (a specific podocyte protein normally associated with the cytoskeleton of foot processes) were increased in this structure; alpha-actinin was especially prominent in the dense bodies. The results are consistent with the view that foot process effacement represents an adaptive change in cell shape including hypertrophy of the contractile apparatus, reinforcing the supportive role of podocytes. Several factors associated with increased distending forces to podocytes may underlie this phenotype change including loss of mesangial support, elevated glomerular pressures, and impairment of GBM substructure as well as of podocyte-GBM-contacts. Twenty-eight days after serum injection a remodeling of the foot process pattern was seen. It appears that this restitution depends on a preceding repair of mesangial support function to glomerular capillaries.

Animals↗
PubMed2005

Antibiotic exposure does not influence MRP2 functional expression in Caco-2 cells.

Multidrug resistance-associated protein 2 (MRP2) is associated with active drug efflux and may influence oral bioavailability of common classes of drugs. MRP2 expression demonstrates plasticity. Caco-2 cells, a routine in vitro model for predicting oral bioavailability, are often cultured in media containing antibiotics. We have investigated whether exposure of Caco-2 cells to two common antibiotic regimes alters MRP2 functional expression. Caco-2 cells were grown in the presence or absence of either gentamicin or penicillin-streptomycin for up to 9 weeks. MRP2 functional activity was assessed by calcein efflux across the apical membrane. MRP2 protein expression was determined by immunoblots. Neither antibiotic regime resulted in consistent changes in calcein efflux across the apical membrane (reflecting MRP2 activity) or basolateral membrane (reflecting MRP3 and possibly MRP6 activity) of Caco-2 cells. MRP2 protein expression also showed no change in response to antibiotic exposure. Routine exposure of Caco-2 cells to penicillin-streptomycin or gentamicin does not affect apical MRP2 functional activity in intestinal enterocytic Caco-2 cells. Extrapolating these results to the situation in vivo suggests that the oral bioavailability of MRP substrates is not predicted to be influenced by recent courses of antibiotics.

Anti-Bacterial Agents↗