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Erythrocyte Membranes (erythrocyte + membrane)

Distribution by Scientific Domains

Medical Sciences	42%
Chemistry	31%
Life Sciences	21%

Selected Abstracts

Cell Adhesion onto Highly Curved Surfaces: One-Step Immobilization of Human Erythrocyte Membranes on Silica Beads

CHEMPHYSCHEM, Issue 7 2003
Stefan Kaufmann
Abstract This paper deals with single-step, orientation-selective immobilization of human erythrocyte membranes on bare silica beads with different topographies: 1) solid (nonporous) silica beads with a diameter of 3 ,m and 2) porous silica beads with a diameter of 5 ,m. Erythrocyte membranes were immobilized onto beads simply by incubation, without sonication or osmotic lysis. Membrane orientation before and after immobilization was identified with two immunofluorescence labels: 1) the extracellular part of glycophorin can be labeled with a first monoclonal antibody and a second polyclonal antibody with fluorescence dyes (outside label), while 2) the cytoplasmic domain of Band 3 can be recognized with a first monoclonal antibody and a second fluorescent polyclonal antibody (inside label). Adherent erythrocytes on the beads all ruptured, inverted the asymmetric orientation of the membrane, and selectively exposed their cytoplasmic domain. The surface topography did not influence the orientation or the amount of immobilized membrane. On the other hand, the fact that no adsorption or rupture of erythrocytes could be observed on planar quartz substrates suggests a significant influence of contact curvature on adhesion energy. [source]

Erythrocyte membranes from a patient with congenital dyserythropoietic anaemia type I (CDA-I) show identical, although less pronounced, glycoconjugate abnormalities to those from patients with CDA-II (HEMPAS)

BRITISH JOURNAL OF HAEMATOLOGY, Issue 4 2000
Ewa Zdebska
Congenital dyserythropoietic anaemias (CDAs) are rare hereditary disorders characterized by ineffective erythropoiesis and multinuclearity of erythroblasts. Three main types of the disease have been described. Glycoconjugate abnormalities in erythrocyte membrane glycoconjugates, consisting of hypoglycosylation of band 3 and accumulation of certain glycosphingolipids including lactotriaosylceramide, neolactotriaosylceramide and polyglycosylceramides, have been described only in patients with CDA type II (CDA-II). We report on identical, although less pronounced, abnormalities in erythrocyte glycoconjugates from a patient with CDA-I. A low degree of hypoglycosylation of band 3 in our patient with CDA-I suggests that hypoglycosylation is not a cause, but, most probably, a consequence of dyserythropoiesis. [source]

Cell Adhesion onto Highly Curved Surfaces: One-Step Immobilization of Human Erythrocyte Membranes on Silica Beads

N-3 polyunsaturated fatty acid diet therapy for patients with inflammatory bowel disease

INFLAMMATORY BOWEL DISEASES, Issue 10 2010
Kan Uchiyama MD
Abstract Background: N-3 polyunsaturated fatty acids (PUFA) are considered important pharmaconutrients for modulating mucosal immunity and therapeutic responses in patients with inflammatory bowel disease (IBD). We investigated the influence of diet therapy involving the use of an "n-3 PUFA food exchange table" (n-3DP) on the fatty acid composition of the erythrocyte membranes of IBD patients and its remission-maintaining effects. Methods: We analyzed the fatty acid composition of the erythrocyte membrane before and after n-3DP intervention in 20 initial-onset IBD patients who had not undergone any dietary intervention. We then analyzed it again and evaluated disease activity after 12,18 months intervention in 230 IBD patients (168 ulcerative colitis, 62 Crohn's disease; follow-up group) in whom n-3DP was introduced after remission had been achieved. The follow-up group was divided into remission and relapse groups. Results: In the 20 initial-onset patients, the mean n-3/n-6 ratio significantly increased after intervention (0.41 ± 0.16 versus 0.70 ± 0.20; P < 0.001). In the follow-up group the ratio in the remission group (n = 145) was significantly higher than that in the relapse group (n = 85) (0.65 ± 0.28 versus 0.53 ± 0.18; P < 0.001). The ratio significantly decreased in those who suffered a relapse after the beginning of treatment (P < 0.01). Conclusions: N-3DP significantly increased the erythrocyte membrane n-3/n-6 ratio in IBD patients, and this ratio was significantly higher in the remission group, suggesting that n-3DP alters the fatty acid composition of the cell membrane and influences clinical activity in IBD patients. (Inflamm Bowel Dis 2010) [source]

Redox Reactions and Electron Transfer Across the Red Cell Membrane

IUBMB LIFE, Issue 7 2003
Eleanor Kennett
Abstract Plasma membrane electron transport systems appear to be ubiquitous. These systems are implicated in hormone signal transduction, cell growth and differentiation events as well as protection from oxidative stress. The red blood cell is constantly exposed to oxidative stress; protection against the reactive species generated during this process may be the main role of its membrane electron transport systems. Membrane redox activity has been studied for over three-quarters of a century, and yet many questions remain regarding its identity and likely roles: are electron transfers by distinct and specific mechanisms; what are the physiological donors and acceptors; and how do these systems affect metabolism? Current evidence suggests that the human erythrocyte membrane contains a number of distinct electron transfer systems, some of which, at least, involve membrane proteins, and NADH or ascorbate as electron donors. The activity of these systems appears to be closely related to the metabolic state of the cell, suggesting that mediation of reducing equivalents across the plasma membrane allows redox buffering of each environment, intra- and extracellular, by the other. We have decided to study this from a new perspective, NMR spectroscopy the area of our own technical expertise, hence this review is slanted towards this more recent analysis. IUBMB Life, 55: 375-385, 2003 [source]

,-cardiac actin (ACTC) binds to the band 3 (AE1) cardiac isoform

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2003
Paulo Roberto Moura Lima
Abstract The band 3 protein is the major integral protein present in the erythrocyte membrane. Two tissue-specific isoforms are also expressed in kidney alpha intercalated cells and in cardiomyocytes. It has been suggested that the cardiac isoform predominantly mediates the anion exchange in cardiomyocytes, but the role of the cytoplasmic domain of the band 3 (CDB3) protein in the cardiac tissue is unknown. In order to characterize novel associations of the CDB3 in the cardiac tissue, we performed the two-hybrid assay, using a bait comprising the region from leu 258 to leu 311 of the erythrocyte band 3, which must also be present in the cardiac isoform. The assay revealed two clones containing the C-terminal region of the ,-cardiac actin. Immunoprecipitation of whole rat heart using an anti-actin antibody, immunoblotted with anti-human band 3, showed that actin binds to band 3 which was confirmed in the reverse assay. The confocal microscopy showed band 3 in the intercalated discs. Thus, besides the in vivo physical interaction in the Saccharomyces cerevisiae cell, we demonstrated using immunopreciptation that there is a physical association of band 3 with ,-cardiac actin in cardiomyocyte, and we suggest that the binding occur "in situ," in the intercalated disc, a site of cell,cell contact and attachment of the sarcomere to the plasma membrane. © 2003 Wiley-Liss, Inc. [source]

Relationships between Na+, K+ -ATPase, sialic acid content and fluidity in rainbow trout density-separated erythrocytes

JOURNAL OF FISH BIOLOGY, Issue 2 2002
E. Salvolini
A correlation was found between membrane fluidity, sialic acid (SA) content and Na+, K+ -ATPase activity in the rainbow trout Oncorhynchus mykiss erythrocyte membrane and this suggests that alterations in erythrocyte Na+, K+ -ATPase activity might be caused by modified membrane fluidity through modified SA content. [source]

Attenuation of ciclosporin-induced nephrotoxicity by dietary supplementation of seal oil in Sprague-Dawley rats

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2005
Wei Yang
Fish oil, rich in omega-3 (n-3) polyunsaturated fatty acids (PUFAs), has been reported to attenuate nephrotoxicity induced by ciclosporin (cyclosporine A). Harp seal oil is a rich source of n-3 PUFAs. This study investigated the ability of dietary seal oil to reduce nephrotoxicity caused by ciclosporin. Sprague-Dawley rats were maintained on a standard diet (with sunflower oil as lipid, SFO) or a diet enriched with seal oil (with 85% seal oil and 15% sunflower oil as lipid, SO) for four weeks before and four weeks after intravenous administration of ciclosporin (15 mg kg,1 daily). Kidney function was assessed by measuring blood urea nitrogen, creatinine clearance, urinary N -acetyl-1-,- d -glucosaminidase, 6-keto-prostaglandin F1,, thromboxane B2 and malondialdehyde. Systolic blood pressure (SBP) was monitored. Ciclosporin concentrations in blood were measured using liquid chromatography-tandem mass spectrometry (LC-MS/MS). The fatty acid compositions of the diets and erythrocyte membranes were analysed by gas chromatography (GC). The results showed that nephrotoxicity was induced by ciclosporin in rats maintained on both SO and SFO diets. However, rats fed on SO diet endured less toxicity than those on SFO diet. The n-3 and n-6 PUFAs in the erythrocyte membrane of rats maintained on SO diet were found to be 10.79% and 11.93%, while those in rats maintained on SFO diet were found to be 1.67% and 22.71%, respectively. In conclusion, dietary supplementation of seal oil was found to reduce ciclosporin-induced nephrotoxicity in rats. [source]

Detection of single lipid bilayers with coherent anti-Stokes Raman scattering (CARS) microscopy

JOURNAL OF RAMAN SPECTROSCOPY, Issue 9 2003
Eric O. Potma
Abstract We investigated vibrational imaging of phospholipid bilayers with CARS microscopy. Single lipid membranes of supported bilayers, giant unilamellar vesicles and intact erythrocyte membrane are detected with the strong resonant signal of the C,H stretching vibration. In addition, it is shown that the CARS signal field of the lipids near the glass/water interface is amplified through mixing with the back-reflected non-resonant CARS field of the glass coverslip. Furthermore, interference effects between two separate bilayers are observed, allowing intermembrane distances to be determined beyond the diffraction-limited resolution of the microscope. Copyright © 2003 John Wiley & Sons, Ltd. [source]

The Maurer's cleft protein MAHRP1 is essential for trafficking of PfEMP1 to the surface of Plasmodium falciparum -infected erythrocytes

MOLECULAR MICROBIOLOGY, Issue 5 2008
Cornelia Spycher
Summary During the intra-erythrocytic development of Plasmodium falciparum, the parasite modifies the host cell surface by exporting proteins that interact with or insert into the erythrocyte membrane. These proteins include the principal mediator of cytoadherence, P. falciparum erythrocyte membrane protein 1 (PfEMP1). To implement these changes, the parasite establishes a protein-trafficking system beyond its confines. Membrane-bound structures called Maurer's clefts are intermediate trafficking compartments for proteins destined for the host cell membrane. We disrupted the gene for the membrane-associated histidine-rich protein 1 (MAHRP1). MAHRP1 is not essential for parasite viability or Maurer's cleft formation; however, in its absence, these organelles become disorganized in permeabilized cells. Maurer's cleft-resident proteins and transit cargo are exported normally in the absence of MAHRP1; however, the virulence determinant, PfEMP1, accumulates within the parasite, is depleted from the Maurer's clefts and is not presented at the red blood cell surface. Complementation of the mutant parasites with mahrp1 led to the reappearance of PfEMP1 on the infected red blood cell surface, and binding studies show that PfEMP1-mediated binding to CD36 is restored. These data suggest an important role of MAHRP1 in the translocation of PfEMP1 from the parasite to the host cell membrane. [source]

Erythrocytes as targets for gamma-glutamyltranspeptidase initiated pro-oxidant reaction

EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 5 2002
Hayet Aberkane
Abstract: Gamma-glutamyltranspeptidase (GGT) is a well known cell plasma membrane and serum circulating enzyme. In clinical chemistry, GGT is used as a marker of alcohol consumption and drug uptake. Serum GGT activity varies in hepatobiliary diseases and cancer. This enzyme is involved in glutathione (GSH) metabolism, which is generally associated with antioxidant properties. However, in recent years, findings from our group and from others showed that GGT-catalysed extracellular metabolism of GSH leads, in the presence of iron, to the generation of reactive oxygen species (ROS). It was demonstrated that those highly reactive species oxidise lipids, cell surface protein thiols or activate transcriptional factors such as Nuclear Factor ,B (NF,B). The objective of the present work is to determine whether the red blood cells are targets for plasma GGT-initiated pro-oxidant reaction. The results obtained demonstrate that the GGT/GSH/iron system oxidises isolated erythrocyte membranes. A significant release of haemoglobin and a decrease of erythrocyte deformability are also observed. In addition, in vivo studies showed a relationship between plasma GGT activity and erythrocyte deformability in 20 studied subjects. In conclusion, GGT-mediated ROS production is able to oxidise erythrocytes and thus disturbs their functions. [source]

Effects of clotrimazole on transport mediated by multidrug resistance associated protein 1 (MRP1) in human erythrocytes and tumour cells

FEBS JOURNAL, Issue 24 2001
Antonios Klokouzas
Clotrimazole has been shown to have potent anti-malarial activity in vitro, one possible mechanism being inhibition of oxidized glutathione (GSSG) export from the infected human red blood cells or from the parasite itself. Efflux of GSSG from normal erythrocytes is mediated by a high affinity glutathione S-conjugate transporter. This paper shows that transport of the model substrate, 3 µm dinitrophenyl S -glutathione, across erythrocyte membranes is inhibited by multidrug resistance-associated protein 1 (MRP1)-specific antibody, QCRL-3, strongly suggesting that the high affinity transport is mediated by MRP1. The rates of transport observed with membrane vesicles prepared from erythrocytes or from multidrug resistant tumour cells show a similar pattern of responses to applied reduced glutathione, GSSG and MRP1 inhibitors (indomethacin, MK571) further supporting the conclusion that the high affinity transporter is MRP1. In both erythrocytes and MRP1-expressing tumour cells, MRP1-associated transport is inhibited by clotrimazole over the range 2,20 µm, and the inhibitory effect leads to increases in accumulation of MRP1 substrates, vincristine and calcein, and decreases in calcein efflux from intact MRP1-expressing human tumour cells. It also results in increased sensitivity to daunorubicin of the multidrug resistant cells, L23/R but not the sensitive parent L23/P cells. These results demonstrate that clotrimazole can inhibit the MRP1 which is present in human erythrocytes, an effect that may contribute to, though not fully account for, its anti-malarial action. [source]

N-3 polyunsaturated fatty acid diet therapy for patients with inflammatory bowel disease

Deficiency of the ,-Subunit of the Stimulatory G Protein and Severe Extraskeletal Ossification,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 11 2000
Mark C. Eddy
Abstract Progressive osseous heteroplasia (POH) is a rare disorder characterized by dermal ossification beginning in infancy followed by increasing and extensive bone formation in deep muscle and fascia. We describe two unrelated girls with typical clinical, radiographic, and histological features of POH who also have findings of another uncommon heritable disorder, Albright hereditary osteodystrophy (AHO). One patient has mild brachydactyly but no endocrinopathy, whereas the other manifests brachydactyly, obesity, and target tissue resistance to thyrotropin and parathyroid hormone (PTH). Levels of the ,-subunit of the G protein (Gs,) were reduced in erythrocyte membranes from both girls and a nonsense mutation (Q12X) in exon 1 of the GNAS1 gene was identified in genomic DNA from the mildly affected patient. Features of POH and AHO in two individuals suggest that these conditions share a similar molecular basis and pathogenesis and that isolated severe extraskeletal ossification may be another manifestation of Gs, deficiency. [source]

Methoxypolyethylene glycol- block -polycaprolactone diblock copolymers reduce P-glycoprotein efflux in the absence of a membrane fluidization effect while stimulating P-glycoprotein ATPase activity

JOURNAL OF PHARMACEUTICAL SCIENCES, Issue 4 2007
Jason Zastre
Abstract We have previously shown that amphiphilic diblock copolymers composed of methoxypolyethylene glycol- b -polycaprolactone (MePEG- b -PCL) increased the cellular accumulation and reduced the basolateral to apical flux of the P-glycoprotein substrate, rhodamine 123 (R-123) in caco-2 cells. The purpose of this study was to investigate membrane perturbation effects of MePEG- b -PCL diblock copolymers with erythrocyte membranes and caco-2 cells and the effect on P-gp ATPase activity. The diblock copolymer MePEG17 -b-PCL5 induced increasing erythrocyte hemolysis at concentrations which correlated with increasing accumulation of R-123 into caco-2 cells. However, no increase in cellular accumulation of R-123 by non-P-gp expressing cells was observed, suggesting that diblock did not enhance the transmembrane passive diffusion of R-123, but that the accumulation enhancement effect of the diblock in caco-2 cells was likely mediated primarily via P-gp inhibition. Fluorescence anisotropy measurements of membrane fluidity and P-gp ATPase activity demonstrated that MePEG17 - b -PCL5 decreased caco-2 membrane fluidity while stimulating ATPase activity approximately threefold at concentrations that maximally enhanced R-123 caco-2 accumulation. These results suggest that inhibition of P-gp efflux by MePEG17 - b -PCL5 does not appear to be related to increases in membrane fluidity or through inhibition in P-gp ATPase activities, which are two commonly reported cellular effects for P-gp inhibition mediated by surfactants. © 2006 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 96: 864,875, 2007 [source]

Attenuation of ciclosporin-induced nephrotoxicity by dietary supplementation of seal oil in Sprague-Dawley rats

Lipid peroxidation, vitamins C, E and reduced glutathione levels in patients with pulmonary tuberculosis

CELL BIOCHEMISTRY AND FUNCTION, Issue 1 2004
M. Vijayamalini
Abstract The present study examined the relationship between lipid peroxidation and vitamin C, vitamin E and reduced glutathione levels in plasma, erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients and an equal number of age-and sex-matched healthy subjects. Enhanced plasma, erythrocytes and erythrocyte membrane lipid peroxidation with concomitant decline in vitamin C, vitamin E and reduced glutathione levels were found in pulmonary tuberculosis patients. The elevated lipid peroxidation and decreased vitamin C, vitamin E and reduced glutathione levels indicate the potential of oxidative damage to erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients. Copyright © 2003 John Wiley & Sons, Ltd. [source]

A Comparison of the Effects of Olopatadine and Ketotifen on Model Membranes

ACTA OPHTHALMOLOGICA, Issue 2000
Howard Brockman
ABSTRACT. Olopatadine is a human conjunctival mast cell stabilizer with anti-histaminic activity. Ketotifen is an older molecule that possesses antihistaminic activity and is reported to have additional pharmacological properties. The interactions of these two compounds with model membranes (i.e., monolayers of 1-stearoyl-2-oleoyl-sn-glycerophosphocholine at the argon-buffer interface), and natural (i.e., erythrocyte) membranes were compared in an effort to understand the differences in their biological activities. Drug-lipid interaction with monolayers was determined by monitoring the surface pressure as a function of the drug concentration in the aqueous phase supporting the monolayer. Drug interaction with erythrocyte membranes was determined by monitoring changes in the permeability of the membranes to hemoglobin and 6-carboxyfluorescein as a function of drug concentration in the medium. Olopatadine and ketotifen are both intrinsically surface active and both interact with phospholipid monolayers. However, in both the presence and absence of lipid monolayers, the changes in surface pressure induced by olopatadine are lower than those caused by ketotifen. The effects of these two drugs on cell membranes were dramatically different. Exposure of bovine erythrocytes to increasing concentrations of ketotifen (1,10 mM) resulted in complete hemolysis of the cells, whereas olopatadine (1,10 mM) caused only minimal hemolysis (<8%). Consistent results were obtained in experiments measuring the leakage of 6-carboxyfluorescein from erythrocyte ghosts as a more sensitive marker of membrane perturbation. Olopatadine treatment (0.1,10 mM) minimally perturbed the cell membrane while ketotifen (1,10 mM) caused a concentration dependent release of the fluorescent marker. These data demonstrate fundamental differences between the two drugs in their effects on cell membranes. Moreover, the differences are consistent with the surface activities of the two compounds measured in monolayers and with reported differences in their pharmacological activities. These findings offer an explanation for the biphasic non-specific cytotoxic effect of ketotifen on histamine release from mast cells and may account for the non-lytic mast cell stabilizing activity of olopatadine. [source]