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1
Walker, Britta, Syeda T. Towhid, Evi Schmid, Sascha M. Hoffmann, Majed Abed, Patrick Münzer, Sebastian Vogel, et al. "Dynamic adhesion of eryptotic erythrocytes to immobilized platelets via platelet phosphatidylserine receptors." American Journal of Physiology-Cell Physiology 306, no. 3 (February 1, 2014): C291—C297. http://dx.doi.org/10.1152/ajpcell.00318.2013.
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Glucose depletion of erythrocytes triggers suicidal erythrocyte death or eryptosis, which leads to cell membrane scrambling with phosphatidylserine exposure at the cell surface. Eryptotic erythrocytes adhere to endothelial cells by a mechanism involving phosphatidylserine at the erythrocyte surface and CXCL16 as well as CD36 at the endothelial cell membrane. Nothing has hitherto been known about an interaction between eryptotic erythrocytes and platelets, the decisive cells in primary hemostasis and major players in thrombotic vascular occlusion. The present study thus explored whether and how glucose-depleted erythrocytes adhere to platelets. To this end, adhesion of phosphatidylserine-exposing erythrocytes to platelets under flow conditions was examined in a flow chamber model at arterial shear rates. Platelets were immobilized on collagen and further stimulated with adenosine diphosphate (ADP, 10 μM) or thrombin (0.1 U/ml). As a result, a 48-h glucose depletion triggered phosphatidylserine translocation to the erythrocyte surface and augmented the adhesion of erythrocytes to immobilized platelets, an effect significantly increased upon platelet stimulation. Adherence of erythrocytes to platelets was blunted by coating of erythrocytic phosphatidylserine with annexin V or by neutralization of platelet phosphatidylserine receptors CXCL16 and CD36 with respective antibodies. In conclusion, glucose-depleted erythrocytes adhere to platelets. The adhesive properties of platelets are augmented by platelet activation. Erythrocyte adhesion to immobilized platelets requires phosphatidylserine at the erythrocyte surface and CXCL16 as well as CD36 expression on platelets. Thus platelet-mediated erythrocyte adhesion may foster thromboocclusive complications in diseases with stimulated phosphatidylserine exposure of erythrocytes.
2
Klotz, F. W., J. D. Chulay, W. Daniel, and L. H. Miller. "Invasion of mouse erythrocytes by the human malaria parasite, Plasmodium falciparum." Journal of Experimental Medicine 165, no. 6 (June 1, 1987): 1713–18. http://dx.doi.org/10.1084/jem.165.6.1713.
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Plasmodium falciparum malaria merozoites require erythrocyte sialic acid for optimal invasion of human erythrocytes. Since mouse erythrocytes have the form of sialic acid found on human erythrocytes (N-acetyl neuraminic acid), mouse erythrocytes were tested for invasion in vitro. The Camp and 7G8 strains of P. falciparum invaded mouse erythrocytes at 17-45% of the invasion rate of human erythrocytes. Newly invaded mouse erythrocytes morphologically resembled parasitized human erythrocytes as shown on Giemsa-stained blood films and by electron microscopy. The rim of parasitized mouse erythrocytes contained the P. falciparum 155-kD protein, which is on the rim of ring-infected human erythrocytes. Camp but not 7G8 invaded rat erythrocytes, indicating receptor heterogeneity. These data suggest that it may be possible to adapt the asexual erythrocytic stage of P. falciparum to rodents. The development of a rodent model of P. falciparum malaria could facilitate vaccine development.
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Murakami, K., and K. Tanabe. "An antigen of Plasmodium yoelii that translocates into the mouse erythrocyte membrane upon entry into the host cell." Journal of Cell Science 73, no. 1 (February 1, 1985): 311–20. http://dx.doi.org/10.1242/jcs.73.1.311.
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Monoclonal antibodies against the rodent malaria parasite, Plasmodium yoelii, have been prepared and characterized by indirect immunofluorescence on acetone-fixed infected mouse erythrocytes. The antibody of clone K2 reacted strongly with late trophozoites and schizonts, whereas it did so weakly and diffusely with ring forms and early trophozoites. Strong fluorescence was confined to granular structures in schizonts and merozoites. Parasites that invaded erythrocytes in vitro lost the strong fluorescence. Instead, immunofluorescence appeared in the membranes of erythrocytes infected in vitro with merozoites. Erythrocytes infected with more than one merozoite had intensified immunofluorescence in their membranes. Staining of the invaded erythrocytes with 4′,6-diamidino-2-phenylindole (DAPI) hydrochloride demonstrated that membranes of all the invaded erythrocytes acquired the P. yoelii antigen. These results suggest that the P. yoelii antigen in merozoites is translocated into erythrocyte membranes upon entry into the host cell. Immunofluorescence continued to appear in membranes of infected erythrocytes throughout the intra-erythrocytic parasite growth. Staining of unfixed infected erythrocytes with the K2 antibody failed to detect the parasite antigen. In contrast, immunofluorescence was present in unfixed membranes of erythrocyte ghosts, which had been spontaneously formed after rupture of schizont-infected erythrocytes by merozoite release. No immunofluorescence appeared in either acetone-fixed or unfixed ghosts of normal erythrocytes. These results suggest the antigenic determinant of the P. yoelii antigen is exposed at the cytoplasmic surface of the infected erythrocyte membrane. Immunoprecipitation has revealed that the K2 antibody recognizes a 160 X 10(3) Mr P. yoelii antigen.
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Reno, Paul W., Katherine Kleftis, Stuart W. Sherburne, and Bruce L. Nicholson. "Experimental Infection and Pathogenesis of Viral Erythrocytic Necrosis (VEN) in Atlantic Cod, Gadus morhua." Canadian Journal of Fisheries and Aquatic Sciences 43, no. 5 (May 1, 1986): 945–51. http://dx.doi.org/10.1139/f86-117.
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Mature Atlantic cod (Gadus morhua) were experimentally infected with viral erythrocytic necrosis (VEN) by inoculation with washed erythrocytes or ceil-free homogenates of erythrocytes from naturally infected fish. Approximately one third of the animals exposed exhibited active infections. The temporal pattern of infection was similar between naturally infected and experimentally infected fish. One to two months after infection, immature erythrocytes began to show clear evidence of VEN followed by a rapid increase in the proportion of infected immature erythrocytes, frequently reaching 100%. A subsequent dramatic drop in infection of immature erythrocytes occurred, coinciding with an increase of infection in mature erythrocytes. Significant erythroblastosis occurred when the overall erythrocyte infection rate reached approximately 10%, but none of the newly generated erythrocytes appeared infected. The peak infection rate (40–60% of erythrocytes infected) declined slowly and the infection, in most instances, was completely resolved.
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Hsiao, L. L., R. J. Howard, M. Aikawa, and T. F. Taraschi. "Modification of host cell membrane lipid composition by the intra-erythrocytic human malaria parasite Plasmodium falciparum." Biochemical Journal 274, no. 1 (February 15, 1991): 121–32. http://dx.doi.org/10.1042/bj2740121.
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The phospholipid and fatty acid compositions of the host infected erythrocyte plasma membrane (IEPM) have been determined for erythrocytes infected with the human malaria parasite Plasmodium falciparum. IEPM were prepared by selective lysis of the host erythrocyte (but not of the parasite membranes) with 0.1% saponin, followed by differential centrifugation. The purity of the IEPM was determined by measuring the membrane-specific enzyme markers acetylcholinesterase, glutamate dehydrogenase and lactate dehydrogenase, and by immunoelectron microscopy using monoclonal antibodies specific for human erythrocyte glycophorin A (4E7) and for a 195 kDa parasite membrane glycoprotein (Pf6 3B10.1). Both approaches demonstrated that the host erythrocyte plasma membrane preparation was free from contamination by parasite membranes. During intra-erythrocytic development of the parasite, the phospholipid composition of the erythrocyte membrane was strikingly altered. IEPM contained more phosphatidylcholine (38.7% versus 31.7%) and phosphatidylinositol (2.1% versus 0.8%) and less sphingomyelin (14.6% versus 28.0%) than normal uninfected erythrocytes. Similar alterations in phospholipid composition were determined for erythrocyte membranes of parasitized cells isolated by an alternative method utilizing polycationic polyacrylamide microbeads (Affigel 731). The total fatty acid compositions of the major phospholipids in IEPM were determined by g.l.c. The percentage of polyunsaturated fatty acids in normal erythrocyte phospholipids (39.4%) was much higher than in phospholipids from purified parasites (23.3%) or IEPM (24.0%). The unsaturation index of phospholipids in IEPM was considerably lower than in uninfected erythrocytes (107.5 versus 161.0) and was very similar to that in purified parasites (107.5 versus 98.5). Large increases in palmitic acid (C16:0) (from 21.88% to 31.21%) and in oleic acid (C18:1) (from 14.64% to 24.60%), and major decreases in arachidonic acid (C20:4) (from 17.36% to 7.85%) and in docosahexaenoic acid (C22:6) (from 4.34% to 1.8%) occurred as a result of infection. The fatty acid profiles of individual phospholipid classes from IEPM resembled in many instances the fatty acid profiles of parasite phospholipids rather than those of uninfected erythrocytes. Analysis of IEPM from P. falciparum-infected erythrocytes (trophozoite stage) revealed that, during intra-erythrocytic maturation of the parasite, the host erythrocyte phospholipid composition was markedly refashioned. These alterations were not dependent on the method used to isolate the IEPM, with similar results obtained using either a saponin-lysis method or binding to Affigel beads. Since mature erythrocytes have negligible lipid synthesis and metabolism, these alterations must occur as a result of parasite-directed metabolism of erythrocyte lipids and/or trafficking of lipids between the parasite and erythrocyte membranes.
6
Lowe-Jinde, L. "Hematological changes in Cryptobia-infected rainbow trout (Salmo gairdneri)." Canadian Journal of Zoology 64, no. 6 (June 1, 1986): 1352–55. http://dx.doi.org/10.1139/z86-201.
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Rainbow trout, Salmo gairdneri, were experimentally infected with Cryptobia salmositica and total and differential erythrocyte and leucocyte abundances were examined. Total erythrocyte counts were profoundly reduced and were lowest at 4 weeks postinoculation during the peak of infection. Differential erythrocyte number showed significant reduction in mature erythrocytes, degenerating erythrocytes, and erythroblasts. The reduction in mature erythrocytes number was observed from 3 through 8 weeks postinoculation, while erythroblast reduction occurred at 1 through 5 weeks postinoculation. Subsequently, the number of erythroblasts increase and reach control values at 6, 7, and 8 weeks postinoculation. Although the total leucocyte count was not significantly changed, the differential leucocyte abundance showed that granulocytes were significantly increased. Similarly, the rarely seen, circulating, immature granuloblasts were increased. Both granuloblast and granulocyte numbers returned to control values by 8 weeks postinoculation. Thus, the pattern of differential erythrocytic and leucocytic changes reflect an acute parasitemia and a subsequent partial recovery of the infected fish to the parasitemia.
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Orwa, Titus Okello, Rachel Waema Mbogo, and Livingstone Serwadda Luboobi. "Mathematical Model for Hepatocytic-Erythrocytic Dynamics of Malaria." International Journal of Mathematics and Mathematical Sciences 2018 (July 2, 2018): 1–18. http://dx.doi.org/10.1155/2018/7019868.
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Human malaria remains a major killer disease worldwide, with nearly half (3.2 billion) of the world’s population at risk of malaria infection. The infectious protozoan disease is endemic in tropical and subtropical regions, with an estimated 212 million new cases and 429,000 malaria-related deaths in 2015. An in-host mathematical model ofPlasmodium falciparummalaria that describes the dynamics and interactions of malaria parasites with the host’s liver cells (hepatocytic stage), the red blood cells (erythrocytic stage), and macrophages is reformulated. By a theoretical analysis, an in-host basic reproduction numberR0is derived. The disease-free equilibrium is shown to be locally and globally asymptotically stable. Sensitivity analysis reveals that the erythrocyte invasion rateβr, the average number of merozoites released per bursting infected erythrocyteK, and the proportion of merozoites that cause secondary invasions at the blood phaseζare the most influential parameters in determining the malaria infection outcomes. Numerical results show that macrophages have a considerable impact in clearing infected red blood cells through phagocytosis. Moreover, the density of infected erythrocytes and hence the severity of malaria are shown to increase with increasing density of merozoites in the blood. Concurrent use of antimalarial drugs and a potential erythrocyte invasion-avoidance vaccine would minimize the density of infected erythrocytes and hence malaria disease severity.
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TUFTS, B. L., R. A. FERGUSON, and R. G. BOUTILIER. "In Vivo and In Vitro Effects of Adrenergic Stimulation on Chloride/Bicarbonate Exchange in Rainbow Trout Erythrocytes." Journal of Experimental Biology 140, no. 1 (November 1, 1988): 301–12. http://dx.doi.org/10.1242/jeb.140.1.301.
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In vitro and in vivo experiments were carried out to determine the effect of catecholamines on erythrocytic chloride/bicarbonate exchange in the rainbow trout. A further modified boat assay is described and was used to measure bicarbonate flux through intact erythrocytes. Catecholamines had no significant effect on the bicarbonate flux in vitro. The erythrocytes were sensitive to adrenergic stimulation, however, since the agonists used caused a decrease in the pH gradient across the erythrocyte membrane. Exhaustive exercise was associated with an increase in bicarbonate flux through the intact erythrocytes. The mechanism for this increase is not clear, but it is evidently not adrenergic in origin.
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SHARMA, A. K., S. N. S. RANDHAWA, S. K. UPPAL, and R. RANJAN. "Changes in haematology, blood mineral profile, ultra structure and superoxide dismutase activities in erythrocytes in hypophosphetemic buffaloes given excess molybdenum." Indian Journal of Animal Sciences 84, no. 5 (May 13, 2014): 516–19. http://dx.doi.org/10.56093/ijans.v84i5.40653.
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Phosphorus deficiency in buffaloes resulted into development of macrocytic, normochromic anaemia with significant decline in haemoglobin, packed cell volume and total erythrocyte count. Erythrocytic superoxide dismutase activity was markedly decreased in hypophosphataemic animals given excess molybdenum (T2) in comparison to hypophosphataemic animals not given molybdenum (T3). Scanning electron microscopy of erythrocytes in both T2 and T3 animals showed presence of spherocytes, discocytes and slight membrane corrugations; while erythrocytes in healthy control (T1) appeared biconcave with mild poikilocytosis. From the present study it can be concluded that phosphorus deficiency induces ultrastructural abnormalities in erythrocyte, which is further aggravated by excess molybdenum supplementation. Increased oxidative damage may contribute structural changes in phosphorus deficiency and molybdenum toxicity.
10
Muenster, Stefan, Arkadi Beloiartsev, Binglan Yu, E. Du, Sabia Abidi, Ming Dao, Gregor Fabry, et al. "Exposure of Stored Packed Erythrocytes to Nitric Oxide Prevents Transfusion-associated Pulmonary Hypertension." Anesthesiology 125, no. 5 (November 1, 2016): 952–63. http://dx.doi.org/10.1097/aln.0000000000001294.
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Abstract Background Transfusion of packed erythrocytes stored for a long duration is associated with increased pulmonary arterial pressure and vascular resistance. Prolonged storage decreases erythrocyte deformability, and older erythrocytes are rapidly removed from the circulation after transfusion. The authors studied whether treating stored packed ovine erythrocytes with NO before transfusion could prevent pulmonary vasoconstriction, enhance erythrocyte deformability, and prolong erythrocyte survival after transfusion. Methods Ovine leukoreduced packed erythrocytes were treated before transfusion with either NO gas or a short-lived NO donor. Sheep were transfused with autologous packed erythrocytes, which were stored at 4°C for either 2 (“fresh blood”) or 40 days (“stored blood”). Pulmonary and systemic hemodynamic parameters were monitored before, during, and after transfusion. Transfused erythrocytes were labeled with biotin to measure their circulating lifespan. Erythrocyte deformability was assessed before and after NO treatment using a microfluidic device. Results NO treatment improved the deformability of stored erythrocytes and increased the number of stored erythrocytes circulating at 1 and 24 h after transfusion. NO treatment prevented transfusion-associated pulmonary hypertension (mean pulmonary arterial pressure at 30 min of 21 ± 1 vs. 15 ± 1 mmHg in control and NO–treated packed erythrocytes, P < 0.0001). Washing stored packed erythrocytes before transfusion did not prevent pulmonary hypertension. Conclusions NO treatment of stored packed erythrocytes before transfusion oxidizes cell-free oxyhemoglobin to methemoglobin, prevents subsequent NO scavenging in the pulmonary vasculature, and limits pulmonary hypertension. NO treatment increases erythrocyte deformability and erythrocyte survival after transfusion. NO treatment might provide a promising therapeutic approach to prevent pulmonary hypertension and extend erythrocyte survival.
11
Kirchgatter, Karin, and Hernando A. Del Portillo. "Clinical and molecular aspects of severe malaria." Anais da Academia Brasileira de Ciências 77, no. 3 (September 2005): 455–75. http://dx.doi.org/10.1590/s0001-37652005000300008.
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The erythrocytic cycle of Plasmodium falciparum presents a particularity in relation to other Plasmodium species that infect man. Mature trophozoites and schizonts are sequestered from the peripheral circulation due to adhesion of infected erythrocytes to host endothelial cells. Modifications in the surface of infected erythrocytes, termed knobs, seem to facilitate adhesion to endothelium and other erythrocytes. Adhesion provides better maturation in the microaerophilic venous atmosphere and allows the parasite to escape clearance by the spleen which recognizes the erythrocytes loss of deformability. Adhesion to the endothelium, or cytoadherence, has an important role in the pathogenicity of the disease, causing occlusion of small vessels and contributing to failure of many organs. Cytoadherence can also describe adhesion of infected erythrocytes to uninfected erythrocytes, a phenomenon widely known as rosetting. Clinical aspects of severe malaria, as well as the host receptors and parasite ligands involved in cytoadherence and rosetting, are reviewed here. The erythrocyte membrane protein 1 of P. falciparum (PfEMP1) appears to be the principal adhesive ligand of infected erythrocytes and will be discussed in more detail. Understanding the role of host receptors and parasite ligands in the development of different clinical syndromes is urgently needed to identify vaccination targets in order to decrease the mortality rates of this disease.
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Kirch, H. J., G. Spates, R. Droleskey, W. J. Kloft, and J. R. DeLoach. "Hemolysis of erythrocytes by the hemolytic system from the blood-feeding stable fly, Stomoxys calcitrans." Proceedings, annual meeting, Electron Microscopy Society of America 50, no. 1 (August 1992): 690–91. http://dx.doi.org/10.1017/s0424820100123854.
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Blood feeding insects have to rely on the protein content of mammalian blood to insure reproduction. A substantial quantity of protein is provided by hemoglobin present in erythrocytes. Access to hemoglobin is accomplished only via erythrocyte lysis. It has been shown that midgut homogenates from the blood feeding stable fly, Stomoxys calcitrans, contain free fatty acids and it was proposed that these detergent-like compounds play a major role as hemolysins in the digestive physiology of this species. More recently sphingomyelinase activity was detected in midgut preparations of this fly, which would provide a potential tool for the enzymatic cleavage of the erythrocyte's membrane sphingomyelin. The action of specific hemolytic factors should affect the erythrocyte's morphology. The shape of bovine erythrocytes undergoing in vitro hemolysis by crude midgut homogenates from the stable fly was examined by scanning and transmission electron microscopy.
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Klei, Thomas, Robin Van Bruggen, Jill Dalimot, Martijn Veldthuis, Erik Mul, Timo Rademakers, Mark Hoogenboezem, et al. "Hemolysis in the Spleen Drives Erythrocyte Turnover." Blood 134, Supplement_1 (November 13, 2019): 946. http://dx.doi.org/10.1182/blood-2019-124342.
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Erythrocytes circulate for an average of 120 days before they are removed from the circulation. Various processes and factors have been identified that may contribute to degradation of senescent erythrocytes, but this complex process is still not completely understood. Accumulation of removal signals such as phosphatidylserine exposure, changes in CD47 expression and oxidation of proteins and lipids that render them susceptible to complement deposition, may contribute to recognition and degradation by red pulp macrophages (RPM) of the spleen. However, many questions remain on the exact mechanisms that determine the fate of aged erythrocytes. This is well exemplified in a mouse study in which physiologically aged erythrocytes were found to undergo phagocytosis by RPM in vivo but not in vitro. This finding suggested that the splenic architecture may play an important role in facilitating erythrocyte turnover. Loss of membrane deformability may lead to the initial trapping of aged or damaged erythrocytes in the spleen, an event that precedes their degradation by macrophages. Loss of deformability can explain why certain genetic diseases that affect erythrocyte membrane deformability, such as is the case in sickle cell disease and spherocytosis, result in trapping in the spleen, giving rise to anaemia. Next to loss of deformability, activation of adhesion molecules, such as Lu/BCAM and CD44, specifically on aged erythrocytes has been proposed to contribute to retention of erythrocytes within the spleen, leading to their turnover. In this study we provide evidence that the splenic environment is of key importance in facilitating erythrocyte turnover through induction of hemolysis. Upon isolating human spleen RPM we noted that only a small proportion of the macrophages were in the process of phagocytosing intact erythrocytes. Based on a range of variables, including the number of erythrocytes that are cleared daily, the number of RPM present in the spleen, the degradation rate of erythrocytes as well as differential contribution of spleen and liver to erythrocyte turnover, conservative estimates approximate that at least a 30-fold fewer erythrophagocytic events are observed in RPM than anticipated. Detailed characterization of erythrocyte and macrophage subpopulations from human spleen tissue led to the identification of a large population of erythrocytes that are devoid of hemoglobin, so-called erythrocyte ghosts. By in vivo imaging of the spleen and transfusion experiments we further confirmed that senescent erythrocytes that are retained in the spleen are subject to hemolysis, thereby forming erythrocyte ghosts. Of note, we found that the levels of haptoglobin and hemopexin, two plasma proteins that are involved in scavenging of haemoglobin and heme, respectively, correlate well with the rate of hemolysis that was observed in the spleen. Additionally, we show that the erythrocyte adhesion molecules which are specifically activated on aged erythrocytes, Lu/BCAM and CD44, cause senescent erythrocytes to interact with the extracellular matrix of the spleen. This adhesion molecule-driven retention of senescent erythrocytes, under low shear conditions, was found to result in steady shrinkage of the erythrocytes and ultimately resulted in hemolysis and ghost formation. In contrast to intact senescent erythrocytes, the remnant erythrocyte ghosts were found to be immediately recognized and rapidly degraded (1-3 hours) by RPM, thereby explaining the lack of phagocytosis of intact erythrocytes in the spleen. Together, these data identify hemolysis and ghost formation as key events in the turnover of senescent erythrocytes, which alters our current understanding of how erythrocyte degradation is regulated. Disclosures No relevant conflicts of interest to declare.
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Magowan, C., RL Coppel, AO Lau, MM Moronne, G. Tchernia, and N. Mohandas. "Role of the Plasmodium falciparum mature-parasite-infected erythrocyte surface antigen (MESA/PfEMP-2) in malarial infection of erythrocytes." Blood 86, no. 8 (October 15, 1995): 3196–204. http://dx.doi.org/10.1182/blood.v86.8.3196.3196.
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Abstract During intraerythrocytic growth of Plasmodium falciparum, several parasite proteins are transported from the parasite to the erythrocyte membrane, where they bind to membrane skeletal proteins. Mature-parasite-infected erythrocyte surface antigen (MESA) has previously been shown to associate with host erythrocyte membrane skeletal protein 4.1. Using a spontaneous mutant of P falciparum that has lost the ability to synthesize MESA and 4.1-deficient erythrocytes, we examined growth of MESA(+) and MESA(-) parasites in normal and 4.1-deficient erythrocytes. Viability of MESA(+) parasites was reduced in 4.1-deficient erythrocytes as compared with that for normal erythrocytes, but MESA(-) parasites grew equally well in 4.1-deficient and normal erythrocytes. Cytoadherence of MESA(+)- and MESA (-)-parasitized normal and 4.1-deficient erythrocytes to C32 melanoma cells was similar, indicating that neither protein 4.1 nor MESA plays a major role in cytoadherence of infected erythrocytes. Localization of MESA in normal and 4.1-deficient erythrocytes was examined by confocal microscopy. MESA was diffusely distributed in the cytosol of 4.1-deficient erythrocytes but was membrane-associated in normal erythrocytes. These findings suggest that MESA binding to protein 4.1 plays a major role in intraerythrocytic parasite viability.
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Magowan, C., RL Coppel, AO Lau, MM Moronne, G. Tchernia, and N. Mohandas. "Role of the Plasmodium falciparum mature-parasite-infected erythrocyte surface antigen (MESA/PfEMP-2) in malarial infection of erythrocytes." Blood 86, no. 8 (October 15, 1995): 3196–204. http://dx.doi.org/10.1182/blood.v86.8.3196.bloodjournal8683196.
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During intraerythrocytic growth of Plasmodium falciparum, several parasite proteins are transported from the parasite to the erythrocyte membrane, where they bind to membrane skeletal proteins. Mature-parasite-infected erythrocyte surface antigen (MESA) has previously been shown to associate with host erythrocyte membrane skeletal protein 4.1. Using a spontaneous mutant of P falciparum that has lost the ability to synthesize MESA and 4.1-deficient erythrocytes, we examined growth of MESA(+) and MESA(-) parasites in normal and 4.1-deficient erythrocytes. Viability of MESA(+) parasites was reduced in 4.1-deficient erythrocytes as compared with that for normal erythrocytes, but MESA(-) parasites grew equally well in 4.1-deficient and normal erythrocytes. Cytoadherence of MESA(+)- and MESA (-)-parasitized normal and 4.1-deficient erythrocytes to C32 melanoma cells was similar, indicating that neither protein 4.1 nor MESA plays a major role in cytoadherence of infected erythrocytes. Localization of MESA in normal and 4.1-deficient erythrocytes was examined by confocal microscopy. MESA was diffusely distributed in the cytosol of 4.1-deficient erythrocytes but was membrane-associated in normal erythrocytes. These findings suggest that MESA binding to protein 4.1 plays a major role in intraerythrocytic parasite viability.
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Wieschhaus, Adam, Anwar Khan, Asma Zaidi, Henry Rogalin, Toshihiko Hanada, Fei Liu, Lucia De Franceschi, Carlo Brugnara, Alicia Rivera, and Athar H. Chishti. "Calpain-1 knockout reveals broad effects on erythrocyte deformability and physiology." Biochemical Journal 448, no. 1 (October 18, 2012): 141–52. http://dx.doi.org/10.1042/bj20121008.
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Pharmacological inhibitors of cysteine proteases have provided useful insights into the regulation of calpain activity in erythrocytes. However, the precise biological function of calpain activity in erythrocytes remains poorly understood. Erythrocytes express calpain-1, an isoform regulated by calpastatin, the endogenous inhibitor of calpains. In the present study, we investigated the function of calpain-1 in mature erythrocytes using our calpain-1-null [KO (knockout)] mouse model. The calpain-1 gene deletion results in improved erythrocyte deformability without any measurable effect on erythrocyte lifespan in vivo. The calcium-induced sphero-echinocyte shape transition is compromised in the KO erythrocytes. Erythrocyte membrane proteins ankyrin, band 3, protein 4.1R, adducin and dematin are degraded in the calcium-loaded normal erythrocytes but not in the KO erythrocytes. In contrast, the integrity of spectrin and its state of phosphorylation are not affected in the calcium-loaded erythrocytes of either genotype. To assess the functional consequences of attenuated cytoskeletal remodelling in the KO erythrocytes, the activity of major membrane transporters was measured. The activity of the K+–Cl− co-transporter and the Gardos channel was significantly reduced in the KO erythrocytes. Similarly, the basal activity of the calcium pump was reduced in the absence of calmodulin in the KO erythrocyte membrane. Interestingly, the calmodulin-stimulated calcium pump activity was significantly elevated in the KO erythrocytes, implying a wider range of pump regulation by calcium and calmodulin. Taken together, and with the atomic force microscopy of the skeletal network, the results of the present study provide the first evidence for the physiological function of calpain-1 in erythrocytes with therapeutic implications for calcium imbalance pathologies such as sickle cell disease.
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Xu, Zhike, Chenyang Wang, Feng He, Pengfei Hao, and Xiwen Zhang. "Coarse-grained model of whole blood hemolysis and morphological analysis of erythrocyte population under non-physiological shear stress flow environment." Physics of Fluids 35, no. 3 (March 2023): 031901. http://dx.doi.org/10.1063/5.0137517.
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Erythrocyte dynamics and hemorheology exist inextricably connection. In order to further explore the population dynamics of erythrocytes in non-physiological shear stress flow and its microscopic hemolysis mechanism, this study improved the coarse-grained erythrocytes damaged model and established the hemoglobin (Hb) diffusion model based on the transport dissipative particle dynamics. The whole blood hemolysis simulation results showed that the red blood cells near the active shear side were more likely to be damaged, and most of the escaping cytoplasm was also concentrated in this side. After the destruction and relaxation of erythrocytes, the cell membrane presents a pathological state of relaxation and swelling. Moreover, we built a deep learning network for recognizing erythrocyte morphology and analyzing the erythrocyte population change rule in non-physiological shear stress flow. In this study, the clues of the blood shear-thinning effect were found from erythrocyte dynamics and coarse-grained simulation. After the shearing starts, the coin-stacked erythrocytes are depolymerized. Then, the overturned double concave erythrocytes changed into multilobe erythrocytes. When the flow shear stress gradually increases, most erythrocytes show an ellipsoidal tank-treading movement along the shear direction. Changes in erythrocyte morphology can reduce flow resistance, showing a phenomenon of the whole blood shear-thinning effect.
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Elblbesy, Mohamed A. "Biomechanical and Physiological Conditions Influence Erythrocytes - Erythrocyte Adhesion. An in vitro Study." Applied Physics Research 9, no. 4 (July 24, 2017): 23. http://dx.doi.org/10.5539/apr.v9n4p23.
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Erythrocyte - erythrocyte adhesion (EEA) is of the large interest since it will effect directly on its function and interaction with other organs. Also, erythrocytes adhesion may arise erythrocytes aggregation which has a significant effect on the hemodynamic mechanism. The present study is aimed at examining the effect of erythrocytes mechanical properties on their adhesion. In addition, the impact of the physiological conditions around erythrocytes on their adhesion will be evaluated. A simple flow compartment technique built on inverted microscope was used to calculate adhesion number (AN) of erythrocytes which reflects the ability of erythrocytes to adhere to each other. AN was correlated strongly to shear rate and erythrocyte deformation index. Shape parameters of erythrocytes (Radius and volume) were found to play a major role in EEA. The concentration of the main plasma proteins (fibrinogen and albumin) were determined to have a significant effect on EEA. The results obtained in this study give the attention that other factors rather than particle diameter and work of adhesion may effect on erythrocytes adhesion.
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Lankin, V. Z., G. G. Konovalova, A. K. Tikhaze, and L. V. Nedosugova. "The influence of natural dicarbonils on the antioxidant enzymes activity in vitro and in vivo." Biomeditsinskaya Khimiya 58, no. 6 (2012): 727–36. http://dx.doi.org/10.18097/pbmc20125806727.
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Natural dicarbonyls, which may be accumulated during oxidative stress in atherosclerosis (e.g. malondialdehyde) or carbonyl stress in diabetes mellitus (glyoxal and methylglyoxal) effectively inhibited the activities of commercial preparations of antioxidant enzymes: catalase, Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and Se-contained glutathione peroxidase from human and bovine erythrocytes and also rat liver glutathione-S-transferase. After incubation of human erythrocytes with 10 mM of each investigated dicarbonyls the decrease of intracellular Cu,Zn-SOD was observed. The decreased activity of erythrocyte Cu,Zn-SOD was also detected in diabetic patients with carbohydrate metabolism disturbance but effective sugar-lowered therapy was accompanied by the increase of this enzyme activity. The increase of erythrocytes activity of Cu,Zn-SOD of diabetic patients theated with metformin (which may utilize methylglyoxal) was higher than in erythrocytase of diabetic patients subjected to traditional therapy.
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Ong, C. W., Z. X. Shen, K. K. H. Ang, U. A. K. Kara, and S. H. Tang. "Raman Microspectroscopy of Normal Erythrocytes and Plasmodium Berghei -Infected Erythrocytes." Applied Spectroscopy 56, no. 9 (September 2002): 1126–31. http://dx.doi.org/10.1366/000370202760295340.
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Raman spectroscopy was applied to study β-haematin, normal erythrocytes, parasite-infected erythrocytes, and lysed samples of the parasite-infected erythrocytes. Differences were observed between spectra excited by the Ar+ laser and those excited by the HeNe laser. The significant difference lies in the fact that with the HeNe laser excitation at 632.8 nm, band absorption is a result of the charge transfer, while laser excitation in Qv-absorption bands of the active site of the haem1 occurs for the Ar+ laser. Similarity in the spectra of β-haematin and parasite-infected erythrocyte was observed with the HeNe laser. The differences between the normal erythrocyte and the parasite-infected erythrocyte may still be distinguished by the band at 754 cm−1 for the parasite-infected erythrocyte. In addition, with the HeNe laser, the band at 1080 cm−1 may also be used as a reference to whether the erythrocyte has been infected.
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Brittain, HA, JR Eckman, RA Swerlick, RJ Howard, and TM Wick. "Thrombospondin from activated platelets promotes sickle erythrocyte adherence to human microvascular endothelium under physiologic flow: a potential role for platelet activation in sickle cell vaso-occlusion." Blood 81, no. 8 (April 15, 1993): 2137–43. http://dx.doi.org/10.1182/blood.v81.8.2137.2137.
Full textAbstract:
Abstract Adherence of erythrocytes to vascular endothelium likely contributes to the pathophysiology of episodic vascular occlusion in patients with sickle cell disease (SCD). In addition, coagulation activation has been reported in sickle patients during complications such as pain episodes. To test the hypothesis that platelet activation contributes to sickle erythrocyte binding, we investigated whether factors released from activated sickle platelets promote adherence of sickle erythrocytes to human microvascular endothelial cells (MEC) under flow conditions. Activated sickle platelet supernatant (ASPS) promoted high levels of sickle erythrocyte adherence to MEC (55.4 +/- 3.9 erythrocytes/mm2) but only moderate adherence of normal erythrocytes to MEC (14.1 +/- 0.7 erythrocytes/mm2). When MEC were incubated with an antibody (OKM5) against CD36 (a thrombospondin [TSP] receptor), platelet supernatant mediated sickle erythrocyte adherence was inhibited 86%, suggesting that TSP participated in the adherence. To further define the role of TSP in adherence, additional studies using purified TSP were performed. At a concentration of 0.2 micrograms/mL TSP in serum-free media (SFM), sickle erythrocyte adherence to MEC was 33.9 +/- 2.7 erythrocytes/mm2 and sixfold greater than either sickle erythrocyte adherence in the absence of TSP or normal erythrocyte adherence in the presence of TSP. Doubling the concentration of TSP to 0.4 micrograms/mL proportionally increased adherence of sickle erythrocytes. Incubation of MEC with OKM5 or anti-alpha v monoclonal antibodies inhibited TSP-mediated sickle erythrocyte adherence more than 95%. These data suggest that activated platelet release factors, including alpha-granule TSP, which promote receptor-mediated sickle erythrocyte adherence to microvascular endothelium. Such factors released during in vivo platelet activation could contribute to vaso-occlusive complications by promoting erythrocyte adherence and microvascular occlusion.
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Brittain, HA, JR Eckman, RA Swerlick, RJ Howard, and TM Wick. "Thrombospondin from activated platelets promotes sickle erythrocyte adherence to human microvascular endothelium under physiologic flow: a potential role for platelet activation in sickle cell vaso-occlusion." Blood 81, no. 8 (April 15, 1993): 2137–43. http://dx.doi.org/10.1182/blood.v81.8.2137.bloodjournal8182137.
Full textAbstract:
Adherence of erythrocytes to vascular endothelium likely contributes to the pathophysiology of episodic vascular occlusion in patients with sickle cell disease (SCD). In addition, coagulation activation has been reported in sickle patients during complications such as pain episodes. To test the hypothesis that platelet activation contributes to sickle erythrocyte binding, we investigated whether factors released from activated sickle platelets promote adherence of sickle erythrocytes to human microvascular endothelial cells (MEC) under flow conditions. Activated sickle platelet supernatant (ASPS) promoted high levels of sickle erythrocyte adherence to MEC (55.4 +/- 3.9 erythrocytes/mm2) but only moderate adherence of normal erythrocytes to MEC (14.1 +/- 0.7 erythrocytes/mm2). When MEC were incubated with an antibody (OKM5) against CD36 (a thrombospondin [TSP] receptor), platelet supernatant mediated sickle erythrocyte adherence was inhibited 86%, suggesting that TSP participated in the adherence. To further define the role of TSP in adherence, additional studies using purified TSP were performed. At a concentration of 0.2 micrograms/mL TSP in serum-free media (SFM), sickle erythrocyte adherence to MEC was 33.9 +/- 2.7 erythrocytes/mm2 and sixfold greater than either sickle erythrocyte adherence in the absence of TSP or normal erythrocyte adherence in the presence of TSP. Doubling the concentration of TSP to 0.4 micrograms/mL proportionally increased adherence of sickle erythrocytes. Incubation of MEC with OKM5 or anti-alpha v monoclonal antibodies inhibited TSP-mediated sickle erythrocyte adherence more than 95%. These data suggest that activated platelet release factors, including alpha-granule TSP, which promote receptor-mediated sickle erythrocyte adherence to microvascular endothelium. Such factors released during in vivo platelet activation could contribute to vaso-occlusive complications by promoting erythrocyte adherence and microvascular occlusion.
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Gruia-Gray, J., and S. S. Desser. "Alterations to the cytoskeleton of erythrocytes infected with frog erythrocytic virus: a fluorescence and electron microscopic study." Biochemistry and Cell Biology 70, no. 2 (February 1, 1992): 123–28. http://dx.doi.org/10.1139/o92-018.
Full textAbstract:
Erythrocytes of bullfrogs (Rana catesbeiana) infected with frog erythrocytic virus are spheroid and their nucleus is displaced. In contrast, uninfected cells are ellipsoid and have a centralized nucleus. Fluorescent staining revealed that these changes are correlated with alterations to components of the erythrocyte cytoskeleton. Uninfected erythrocytes contained a broad, continuous marginal band of microtubules, which appeared thinner and interrupted in infected cells. The described disruption of microtubules was associated with an inability to polymerize the tubulin pool with the addition of 12 μM taxol. The arrangement of submembranous microfilaments in uninfected erythrocytes was not significantly altered in infected cells. Vimentin filaments were distributed throughout the cytoplasm and around the nucleus of uninfected cells, and concentrated at the cell and nuclear peripheries. Cytoplasmic pockets that did not contain vimentin filaments were associated with the viral assembly site(s) in infected cells. These data suggest that the distortion of viral-infected erythrocytes could be due, in part, to an irreversible depolymerization of microtubules of the marginal band and a reorganization of the vimentin filament network.Key words: fluorescence microscopy, Rana catesbeiana, tubulin, vimentin, viral assembly sites.
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Murphy, Sean C., Souvik Bhattacharjee, Travis Harrison, and Kasturi Haldar. "Accessing the Erythrocyte Cytoplasm: A Method for Manipulating the Intracellular Environment of Erythrocytes for the Study of Malaria Invasion, Trafficking and Growth." Blood 104, no. 11 (November 16, 2004): 3688. http://dx.doi.org/10.1182/blood.v104.11.3688.3688.
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Abstract Invasion of erythrocytes by malaria parasites requires participation of both parasite ligands and host determinants. Further recent studies show that erythrocyte G protein signaling regulates malarial infection. Many of the Gs-associated signaling components reside on the cytoplasmic leaflet of the erythrocyte plasma membrane, rendering them inaccessible to most extracellular probes. Since erythrocytes are enucleated and terminally differentiated, they cannot be transfected to express exogenous transgenes. We have modified methods of hypotonic lysis and isotonic resealing to generate loaded erythrocyte ghosts that can be efficiently infected by Plasmodium falciparum and sustain normal levels of intraerythrocytic parasite growth and replication. Further, we show that these ghosts can be filled with various membrane-impermeable peptides or other proteinaceous cargoes for studying signaling and transport events inside the erythrocyte. Resealed ghosts morphologically resemble normal erythrocytes, albeit with reduced hemoglobin content. Other measures of erythrocyte function and malarial infection are being investigated. Studies will be presented on the use of ‘reconstituted’ erythrocytes in elucidating mechanisms parasite invasion as well as parasite protein trafficking in erythrocytes infected by P. falciparum.
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Akel, Ahmad, Carsten A. Wagner, Jana Kovacikova, Ravi S. Kasinathan, Valentin Kiedaisch, Saisudha Koka, Seth L. Alper, et al. "Enhanced suicidal death of erythrocytes from gene-targeted mice lacking the Cl−/HCO3−exchanger AE1." American Journal of Physiology-Cell Physiology 292, no. 5 (May 2007): C1759—C1767. http://dx.doi.org/10.1152/ajpcell.00158.2006.
Full textAbstract:
Genetic defects of anion exchanger 1 (AE1) may lead to spherocytic erythrocyte morphology, severe hemolytic anemia, and/or cation leak. In normal erythrocytes, osmotic shock, Cl−removal, and energy depletion activate Ca2+-permeable cation channels with Ca2+-induced suicidal erythrocyte death, i.e., surface exposure of phosphatidylserine, cell shrinkage, and membrane blebbing, all features typical for apoptosis of nucleated cells. The present experiments explored whether AE1 deficiency favors suicidal erythrocyte death. Peripheral blood erythrocyte numbers were significantly smaller in gene-targeted mice lacking AE1 ( AE1−/−mice) than in their wild-type littermates ( AE1+/+mice) despite increased percentages of reticulocytes ( AE1−/−: 49%, AE1+/+: 2%), an indicator of enhanced erythropoiesis. Annexin binding, reflecting phosphatidylserine exposure, was significantly larger in AE1−/−erythrocytes/reticulocytes (∼10%) than in AE1+/+erythrocytes (∼1%). Osmotic shock (addition of 400 mM sucrose), Cl−removal (replacement with gluconate), or energy depletion (removal of glucose) led to significantly stronger annexin binding in AE1−/−erythrocytes/reticulocytes than in AE1+/+erythrocytes. The increase of annexin binding following exposure to the Ca2+ionophore ionomycin (1 μM) was, however, similar in AE1−/−and in AE1+/+erythrocytes. Fluo3 fluorescence revealed markedly increased cytosolic Ca2+permeability in AE1−/−erythrocytes/reticulocytes. Clearance of carboxyfluorescein diacetate succinimidyl ester-labeled erythrocytes/reticulocytes from circulating blood was more rapid in AE1−/−mice than in AE1+/+mice and was accelerated by ionomycin treatment in both genotypes. In conclusion, lack of AE1 is associated with enhanced Ca2+entry and subsequent scrambling of cell membrane phospholipids.
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Naparlo, Katarzyna, Grzegorz Bartosz, Ireneusz Stefaniuk, Bogumil Cieniek, Miroslaw Soszynski, and Izabela Sadowska-Bartosz. "Interaction of Catechins with Human Erythrocytes." Molecules 25, no. 6 (March 24, 2020): 1456. http://dx.doi.org/10.3390/molecules25061456.
Full textAbstract:
The aim of this study was to characterize the interaction of chosen catechins ((+)-catechin, (−)-epigallocatechin (EGC), and (−)-epigallocatechin gallate (EGCG)) with human erythrocytes and their protective effects against oxidative damage of erythrocytes. Uptake of the catechins by erythrocytes was studied by fluorimetry, their interaction with erythrocyte membrane was probed by changes in erythrocyte osmotic fragility and in membrane fluidity evaluated with spin labels, while protection against oxidative damage was assessed by protection against hemolysis induced by permanganate and protection of erythrocyte membranes against lipid peroxidation and protein thiol group oxidation. Catechin uptake was similar for all the compounds studied. Accumulation of catechins in the erythrocyte membrane was demonstrated by the catechin-induced increase in osmotic resistance and rigidification of the erythrocyte membrane detected by spin labels 5-doxyl stearic acid and 16-doxyl stearic acid. (−)-Epigallocatechin and EGCG inhibited erythrocyte acetylcholinesterase (mixed-type inhibition). Catechins protected erythrocytes against permanganate-induced hemolysis, oxidation of erythrocyte protein thiol groups, as well as membrane lipid peroxidation. These results contribute to the knowledge of the beneficial effects of catechins present in plant-derived food and beverages.
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DeLoach, JR, and GG Wagner. "Some Effects of the Trypanocidal Drug Isometamidium on Encapsulation in Bovine Carrier Erythrocytes." Biotechnology and Applied Biochemistry 10, no. 5 (October 1988): 447–53. http://dx.doi.org/10.1111/j.1470-8744.1988.tb00035.x.
Full textAbstract:
Bovine erythrocyte exposure to isometamidium chloride causes increased osmotic fragility. Control cells tolerated up to 1 mg/ml drug with no effects. Carrier erythrocytes were highly susceptible to drug, with increased osmotic fragility and decreased encapsulation potential of sucrose and inulin. Scanning electron micrographs of control and carrier erythrocytes exposed to drug revealed the formation of enkephalocytes with carrier erythrocytes. Control erythrocytes showed greater tolerance to the drug. Apparently, access of the drug to the interior of the erythrocyte membrane allows the drug to be more interactive with the membrane.
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Doubrovski V. A., Torbin S.O., and Zabenkov I.V. "Determination of individual and average characteristics of native blood erythrocytes by the static spectral digital microscopy method." Optics and Spectroscopy 130, no. 6 (2022): 709. http://dx.doi.org/10.21883/eos.2022.06.54708.29-22.
Full textAbstract:
The method of static (non-flow) spectral digital microscopy (SSDM) method to identify, to count and to determine the standard and individual characteristics of native blood erythrocytes is suggested. The object to study was the whole donor blood diluted by saline and placed into the counting Goryaev camber. Among the standard characteristics of erythrocytes, the following were determined: the concentration of erythrocytes in a blood sample RBC (Red Blood Cells concentration), the scatter of erythrocytes by volume RDW (Red cells Distribution Width), including RDW-SD and RDW-CV, hematocrit HCT, mean erythrocyte volume MCV (Mean Cell Volume). n addition, the possibility of measuring the average hemoglobin content in erythrocyte MCH (Mean Cell Hemoglobin), MCHC (Mean Corpuscular Hemoglobin Concentration), as well as the total content of hemoglobin HGB in the blood sample (Hemoglobin) was investigated. The peculiarity of SSCM method proposed lies in the fact that it fundamentally allows to determine not only the general hematological characteristics of blood samples (RBC, RDW-SD and RDW-CV, HGB), but also the mean values of the characteristics of native blood erythrocytes (MCV, MCH, MCHC), and also, and most importantly, the individual characteristics of each erythrocyte. The latter permitted the authors to introduce a new type of erythrocyte characteristics ICV, ICH, ICHC (Individual Cell Volume, Individual Cell Hemoglobin, Individual Corpuscular Hemoglobin Concentration). In turn, this made it possible to obtain the histograms of hemoglobin distribution in erythrocytes of a blood sample along with the traditional distribution of their volumes, which can serve as an additional tool in the field of hemodiagnostics. Thus, the paper shows that SSCM method makes it possible to compile an individual metrological "passport" for each erythrocyte of the blood sample under study --- this is the main feature of this work. Keywords: erythrocyte identification, erythrocyte counting, individual characteristics of erythrocytes, static spectral digital microscopy.
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Bereznyakov, V. I. "Erythrocytes and Their Importance in the Pathogenesis of Community-Acquired Pneumonia." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 7, no. 1 (March 22, 2022): 86–90. http://dx.doi.org/10.26693/jmbs07.01.086.
Full textAbstract:
The purpose of the study was to study the response of erythrocytes in patients with community-acquired pneumonia and to assess its importance in the pathogenesis of this disease. Materials and methods. Thirty patients with community-acquired pneumonia were examined. The diagnosis was established on the basis of epidemiological, clinical, laboratory, radiological data. Erythrocyte count, hemoglobin concentration, hematocrit number, erythrocyte indexes were determined: mean erythrocyte volume, mean hemoglobin content in erythrocyte, mean hemoglobin concentration in erythrocyte. Results and discussion. It is established that with community-acquired pneumonia in the body there is an increase in the formation of reactive oxygen species at all times of observation. The study of the qualitative and quantitative composition of blood cells in our study found significant shifts in all indicators. Thus, the number of erythrocytes on the 1st day of observation increased by 20.9% relative to the group of healthy individuals, and then decreased and remained by 8 % – 10 % less than in the control on the 5th day. Subsequently, after 10 days there was a sharp (2.2 times) decrease in the number of erythrocytes. However, in general, the concentration of erythrocytes in this observation period remained significantly reduced relative to the group of almost healthy individuals by 20%. Changes in hemoglobin concentration had a similar dynamic. The maximum decrease in erythrocytes count and hemoglobin concentration in the blood over time indicates active hemolysis of erythrocytes during this period. Hematocrit in the examined patients increased sharply on the 1st day of the study, which indicated blood clotting. However, on day 5, hematocrit decreased sharply, amounting to only 57% of the level of the practically healthy individuals’ group and practically did not recover to the ascending level on the 10th day. The mean erythrocyte volume did not change significantly during the study. Conclusion. Changes in the number of erythrocytes, hemoglobin and erythrocyte indices in community-acquired pneumonia are due to membrane-destructive processes in erythrocytes, a decrease in their absolute number – due to hemolysis, hematocrit changes – due to redistribution of blood and hypoxia that develops in non-hospital pneumonia. Changes in erythrocytes are oxygen-dependent mechanisms in the pathogenesis of community-acquired pneumonia
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Davies, A. J., and N. R. Merrett. "Presumptive Viral Erythrocytic Necrosis in the Benthopelagic Fish Coryphaenoides (Nematonurus) Armatus from the Abyss West Of Portugal." Journal of the Marine Biological Association of the United Kingdom 78, no. 3 (August 1998): 1031–34. http://dx.doi.org/10.1017/s0025315400045008.
Full textAbstract:
Presumptive viral erythrocytic necrosis (VEN) was recorded from 1/4 of the benthopelagic fish Coryphaenoides (Nematonurus) armatus (Teleostei: Macrouridae) trawled from the abyss west of Portugal. In a blood smear made from the caudal vein of this fish, 8·6% of erythrocytes contained 1–2 intracytoplasmic inclusions which were invariably round and 1·13 ±0·43 μm in diameter. An eosinophilic granular area accompanied many inclusions. In comparison with erythrocytes from uninfected specimens of C. (N.) armatus, most of those from the infected fish were larger. Erythrocytes with suspected VEN exhibited either normal staining, or were pale, with swollen or crenated nuclei which were often displaced to the cell periphery. Erythrocyte ghosts, with and without inclusions and granules, were present in the same infected fish, suggesting osmotic damage to red cells resulting from the infection. None of 13 other C. (N.) armatus and 27 fish examined from collections made south of Maderia, representing another 20 species of benthic, benthopelagic and mid-water fish, had detectable infections.
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Schreiber, Arnd, Volker Storch, Martin Powilleit, and Robert P. Higgins. "The blood of Halicryptus spinulosus (Priapulida)." Canadian Journal of Zoology 69, no. 1 (January 1, 1991): 201–7. http://dx.doi.org/10.1139/z91-030.
Full textAbstract:
The blood of the priapulid Halicryptus spinulosus was investigated by protein electrophoresis and electron microscopy. Two cell types were encountered: irregularly shaped amoebocytes and spherical erythrocytes. In vitro, the former efficiently phagocytized bacteria and tended to coagulate. A 12-kilodalton polypeptide was the major molecule in erythrocytes, amounting to 20–30% of total erythrocytic proteins. It contained iron and probably formed complexes of higher molecular mass in the cells. These findings support suggestions that Halicryptus contains a haemerythrin-like pigment. Blood colour ranged from pink to black, probably depending on the hydrogen sulphide or oxygen concentration of the medium. Haematocrit values averaged 15.6%, and 58 000 erythrocytes were typically counted per microlitre of body fluid. The major blood constituent was a water-clear serum containing at least 20 proteins at very low and fairly variable concentrations; the molecular masses have been determined for 14 of these. A 46-kilodalton protein was prominent among serum proteins. Superoxide dismutase activity was demonstrated in erythrocyte lysates.
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Sblano, Cesare, Silvia Micelli, and Daniela Meleleo. "Effects of n-Octyl-β-D-Glucopyranoside on Human and Rat Erythrocyte Membrane Stability Against Hemolysis." Open Biology Journal 5, no. 1 (April 11, 2012): 1–5. http://dx.doi.org/10.2174/1874196701205010001.
Full textAbstract:
The practical importance for the pharmaceutical and cosmetics industries of the interactions between biological membranes and surfactant molecules has led to intensive research within this area. The interactions of non-ionic surfactant n-octyl-β-D-glucopyranoside (OG) with the human and rat erythrocyte membranes were studied. The in vitro hemolytic and antihemolytic activities were determined by employing a method in which both erythrocytes were added to the hypotonic medium containing OG at different concentrations, and the amount of haemoglobin released was determined. noctyl- β-D-glucopyranoside was found to have a biphasic effect on both types of erythrocyte membrane. We also investigated the interactions of OG with the erythrocyte membrane in isotonic medium; the dose-dependent curves show similar behaviour in both human and rat erythrocytes. Our results showed that OG has greater antihemolytic potency on rat than on human erythrocytes; furthermore, rat erythrocytes were more sensitive than human erythrocytes to hypotonic shock. How the different lipoprotein structure of these erythrocytes determines a difference in antihemolytic activity is discussed.
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Zhang, Dongyan, Junko Takahashi, Taiko Seno, Yoshihiko Tani, and Takeshi Honda. "Analysis of Receptor for Vibrio choleraeEl Tor Hemolysin with a Monoclonal Antibody That Recognizes Glycophorin B of Human Erythrocyte Membrane." Infection and Immunity 67, no. 10 (October 1, 1999): 5332–37. http://dx.doi.org/10.1128/iai.67.10.5332-5337.1999.
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ABSTRACT El Tor hemolysin (ETH), a pore-forming toxin secreted byVibrio cholerae O1 biotype El Tor and most Vibrio cholerae non-O1 isolates, is able to lyse erythrocytes and other mammalian cells. To study the receptor for this toxin or the related molecule(s) on erythrocyte, we first isolated a monoclonal antibody, B1, against human erythrocyte membrane, which not only blocks the binding of ETH to human erythrocyte but also inhibits the hemolytic activity of ETH. Biochemical characterization and immunoblotting revealed that this antibody recognized an epitope on the extracellular domain of glycophorin B, a sialoglycoprotein of erythrocyte membrane. Erythrocytes lacking glycophorin B but not glycophorin A were less sensitive to the toxin than were normal human erythrocytes. These results indicate that glycophorin B is a receptor for ETH or at least an associated molecule of the receptor for ETH on human erythrocytes.
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Klei, Thomas R. L., Jill J. Dalimot, Boukje M. Beuger, Martijn Veldthuis, Fatima Ait Ichou, Paul J. J. H. Verkuijlen, Iris M. Seignette, et al. "The Gardos effect drives erythrocyte senescence and leads to Lu/BCAM and CD44 adhesion molecule activation." Blood Advances 4, no. 24 (December 16, 2020): 6218–29. http://dx.doi.org/10.1182/bloodadvances.2020003077.
Full textAbstract:
Abstract Senescence of erythrocytes is characterized by a series of changes that precede their removal from the circulation, including loss of red cell hydration, membrane shedding, loss of deformability, phosphatidyl serine exposure, reduced membrane sialic acid content, and adhesion molecule activation. Little is known about the mechanisms that initiate these changes nor is it known whether they are interrelated. In this study, we show that Ca2+-dependent K+ efflux (the Gardos effect) drives erythrocyte senescence. We found that increased intracellular Ca2+ activates the Gardos channel, leading to shedding of glycophorin-C (GPC)–containing vesicles. This results in a loss of erythrocyte deformability but also in a marked loss of membrane sialic acid content. We found that GPC-derived sialic acid residues suppress activity of both Lutheran/basal cell adhesion molecule (Lu/BCAM) and CD44 by the formation of a complex on the erythrocyte membrane, and Gardos channel–mediated shedding of GPC results in Lu/BCAM and CD44 activation. This phenomenon was observed as erythrocytes aged and on erythrocytes that were otherwise prone to clearance from the circulation, such as sickle erythrocytes, erythrocytes stored for transfusion, or artificially dehydrated erythrocytes. These novel findings provide a unifying concept on erythrocyte senescence in health and disease through initiation of the Gardos effect.
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Campanella, M. Estela, Haiyan Chu, Nancy J. Wandersee, Luanne L. Peters, Narla Mohandas, Diana M. Gilligan, and Philip S. Low. "Characterization of glycolytic enzyme interactions with murine erythrocyte membranes in wild-type and membrane protein knockout mice." Blood 112, no. 9 (November 1, 2008): 3900–3906. http://dx.doi.org/10.1182/blood-2008-03-146159.
Full textAbstract:
Previous research has shown that glycolytic enzymes (GEs) exist as multienzyme complexes on the inner surface of human erythrocyte membranes. Because GE binding sites have been mapped to sequences on the membrane protein, band 3, that are not conserved in other mammalian homologs, the question arose whether GEs can organize into complexes on other mammalian erythrocyte membranes. To address this, murine erythrocytes were stained with antibodies to glyceraldehyde-3-phosphate dehydrogenase, aldolase, phosphofructokinase, lactate dehydrogenase, and pyruvate kinase and analyzed by confocal microscopy. GEs were found to localize to the membrane in oxygenated erythrocytes but redistributed to the cytoplasm upon deoxygenation, as seen in human erythrocytes. To identify membrane proteins involved in GE assembly, erythrocytes from mice lacking each of the major erythrocyte membrane proteins were examined for GE localization. GEs from band 3 knockout mice were not membrane associated but distributed throughout the cytoplasm, regardless of erythrocyte oxygenation state. In contrast, erythrocytes from mice lacking α-spectrin, ankyrin, protein 4.2, protein 4.1, β-adducin, or dematin headpiece exhibited GEs bound to the membrane. These data suggest that oxygenation-dependent assembly of GEs on the membrane could be a general phenomenon of mammalian erythrocytes and that stability of these interactions depends primarily on band 3.
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Yokoyama, Naoaki, Boonchit Suthisak, Haruyuki Hirata, Tomohide Matsuo, Noboru Inoue, Chihiro Sugimoto, and Ikuo Igarashi. "Cellular Localization of Babesia bovis Merozoite Rhoptry-Associated Protein 1 and Its Erythrocyte-Binding Activity." Infection and Immunity 70, no. 10 (October 2002): 5822–26. http://dx.doi.org/10.1128/iai.70.10.5822-5826.2002.
Full textAbstract:
ABSTRACT The cellular localization of Babesia bovis rhoptry-associated protein 1 (RAP-1) and its erythrocyte-binding affinity were examined with anti-RAP-1 antibodies. In an indirect immunofluorescent antibody test, RAP-1 was detectable in all developmental stages of merozoites and in extracellular merozoites. In the early stage of merozoite development, RAP-1 appears as a dense accumulation, which later thins out and blankets the host cell cytoplasm, but retains a denser mass around newly formed parasite nuclei. The preferential accumulations of RAP-1 on the inner surface of a host cell membrane and bordering the parasite's outer surface were demonstrable by immunoelectron microscopy. An erythrocyte-binding assay with the lysate of merozoites demonstrated RAP-1 binding to both bovine and equine erythrocytes. Anti-RAP-1 monoclonal antibody 1C1 prevented the interaction of RAP-1 with bovine erythrocytes and significantly inhibited parasite proliferation in vitro. With the recombinant RAP-1, the addition of increasing concentrations of Ca2+ accentuated its binding affinity with bovine erythrocytes. The present findings lend support to an earlier proposition of an erythrocytic binding role for RAP-1 expressed in B. bovis merozoites and, possibly, its involvement in the escape of newly formed merozoites from host cells.
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JAKEMAN, G. N., A. SAUL, W. L. HOGARTH, and W. E. COLLINS. "Anaemia of acute malaria infections in non-immune patients primarily results from destruction of uninfected erythrocytes." Parasitology 119, no. 2 (August 1999): 127–33. http://dx.doi.org/10.1017/s0031182099004564.
Full textAbstract:
While anaemia has long been recognized as a consequence of acute infections with malaria, the relative contributions of direct erythrocyte destruction by parasites, destruction of uninfected erythrocytes and changes in erythropoiesis have been unclear. Fitting of parasitaemia and anaemia data from neurosyphilis patients undergoing malaria therapy to a mathematical model shows that in these patients, an average of 8·5 erythrocytes were destroyed in addition to each erythrocyte observed to become parasitized. The model also showed that dyserythropoiesis plays an insignificant role in the resulting anaemia. The anaemia occurs before a substantial antibody response to parasites or erythrocytes could be generated. We postulate that uninfected erythrocyte destruction occurs through phagocytosis of erythrocytes bound to merozoites killed as a result of the accompanying malaria paroxysms.
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Mikaelyan, Marieta S., Mariam A. Shahinyan, Gayane H. Poghosyan, Evelina G. Sargsyan, and Anahit V. Nerkararyan. "STUDY OF ASPIRIN EFFECT ON STABILITY OF MEMBRANES OF RAT BLOOD ERYTHROCYTES BY ACIDIC HEMOLYSIS METHOD." Proceedings of the YSU B: Chemical and Biological Sciences 56, no. 1 (257) (May 3, 2022): 56–62. http://dx.doi.org/10.46991/pysu:b/2022.56.1.056.
Full textAbstract:
In this work the effect of aspirin on stability of rat blood erythrocyte membranes was studied, using acidic hemolysis method. Hemolysis rate of erythrocytes was shown to depend on preservation time of rat erythrocyte suspension. With increasing of preservation time the original value of optic density of rat erythrocyte suspension decreases and hemolysis time reduces. It was also shown that in the presence of aspirin the membrane stability of low-stable erythrocytes increases, moreover, hemolysis duration enhances, while aspirin leads to decreasing of membrane stability of both high-stable and enhanced-stable erythrocytes of rats.
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Kostic, Ivana, Vesna Ilic, Katarina Bukara, Slavko Mojsilovic, Zorka Djuric, Petra Draskovic, and Branko Bugarski. "Flow cytometric determination of osmotic behaviour of animal erythrocytes toward their engineering for drug delivery." Chemical Industry 69, no. 1 (2015): 67–76. http://dx.doi.org/10.2298/hemind140124021k.
Full textAbstract:
Despite the fact that the methods based on the osmotic properties of the cells are the most widely used for loading of drugs in human and animal erythrocytes, data related to the osmotic properties of erythrocytes derived from animal blood are scarce. This work was performed with an aim to investigate the possibility of use the flow cytometry as a tool for determination the osmotic behaviour of porcine and bovine erythrocytes, and thus facilitate the engineering of erythrocytes from animal blood to be drug carriers. The method of flow cytometry successfully provided the information about bovine and porcine erythrocyte osmotic fragility, and made the initial steps in assessment of erythrocyte shape in a large number of erythrocytes. Although this method is not able to confirm the swelling of pig erythrocytes, it indicated to the differences in pig erythrocytes that had basic hematological parameters inside and outside the reference values. In order to apply/use the porcine and bovine erythrocytes as drug carriers, the method of flow cytometry, confirming the presence of osmotically different fractions of red blood cells, indicated that various amounts of the encapsulated drug in porcine and bovine erythrocytes can be expected.
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Khmil, N. V., O. L. Altuhov, V. G. Kolesnikov, and O. O. Altuhov. "Visualization Of Cell Signal Transduction By The Method Of Microwave Dielectrometry At Dilated Cardiomyopathy." Bionics of Intelligence 1, no. 94 (June 2, 2020): 91–99. http://dx.doi.org/10.30837/bi.2020.1(94).14.
Full textAbstract:
The results of processing the transduction of the cell signal in erythrocytes under physiological conditions and duringdevelopment of dilated cardiomyopathy are presented. The microwave dielectrometry method was tested to visualize the electromagnetic signal from a suspension of erythrocytes using the “sweep”-regime of a piezoelectric cell in the sound frequency range f=10÷12000 Hz. Erythrocyte hydration was estimated by the parameter of the real part of the complex permittivity e′ at a frequency of 37.7 GHz. The use of a stimulator and modulator of β-adrenergic receptors – adrenaline and prostaglandin E2 allowed us to simulate a violation in the system of transduction of the cell signal through the adenylate cyclase system of erythrocytes in vitro. Analysis of the erythrocyte’s electromagnetic response spectra in the “sweep”-regime recorded differences in the intact and experimental samples, as well as during the screening of the additives used. The dielectric data were verified with the data of echocardiography and radiography, which made it possible to recommend microwave dielectrometry as one of the methods of non-invasive operative diagnosis of dilated cardiomyopathy
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Burger, Patrick, Petra Hilarius-Stokman, Dirk de Korte, Timo K. van den Berg, and Robin van Bruggen. "CD47 functions as a molecular switch for erythrocyte phagocytosis." Blood 119, no. 23 (June 7, 2012): 5512–21. http://dx.doi.org/10.1182/blood-2011-10-386805.
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Abstract CD47 on erythrocytes inhibits phagocytosis through interaction with the inhibitory immunoreceptor SIRPα expressed by macrophages. Thus, the CD47-SIRPα interaction constitutes a negative signal for erythrocyte phagocytosis. However, we report here that CD47 does not only function as a “do not eat me” signal for uptake but can also act as an “eat me” signal. In particular, a subset of old erythrocytes present in whole blood was shown to bind and to be phagocytosed via CD47-SIRPα interactions. Furthermore, we provide evidence that experimental aging of erythrocytes induces a conformational change in CD47 that switches the molecule from an inhibitory signal into an activating one. Preincubation of experimentally aged erythrocytes with human serum before the binding assay was required for this activation. We also demonstrate that aged erythrocytes have the capacity to bind the CD47-binding partner thrombospondin-1 (TSP-1) and that treatment of aged erythrocytes with a TSP-1–derived peptide enabled their phagocytosis by human red pulp macrophages. Finally, CD47 on erythrocytes that had been stored for prolonged time was shown to undergo a conformational change and bind TSP-1. These findings reveal a more complex role for CD47-SIRPα interactions in erythrocyte phagocytosis, with CD47 acting as a molecular switch for controlling erythrocyte phagocytosis.
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Smeets, Michel WJ, Alexander PJ Vlaar, Herm Jan M. Brinkman, Jan J. Voorberg, and Peter L. Hordijk. "Platelet-Independent Adhesion of Red Blood Cells to Von Willebrand Factor." Blood 124, no. 21 (December 6, 2014): 2769. http://dx.doi.org/10.1182/blood.v124.21.2769.2769.
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Abstract Background/Objectives Red blood cell (RBC) transfusion can be lifesaving and is an essential therapy in conditions associated with tissue hypoxia due to anemia. However, recent clinical studies show that both the number of RBCs and the age of RBCs transfused are independent risk factors for an increase in transfusion related morbidity and mortality. It has been suggested that the so called “storage lesion” of RBCs, a reduction of quality of erythrocytes and changes in the erythrocyte concentrate storage medium, is the causal factor. Recently it has been shown that cold storage of erythrocytes induces microparticle formation. These erythrocyte microparticles are pro-coagulant and can cause thrombin formation. Another phenomenon of the storage lesion is the rapid and considerable loss of donor erythrocytes from the circulation of transfused patients. We wondered whether thrombin generated by transfused erythrocyte microparticles could contribute to red blood cell adherence to the vascular endothelium. Cytoadherence of red blood cells could contribute to the loss of circulating transfused red blood cells and vascular obstruction and could explain the observed transfusion associated complications in clinical practice. Methods/Results Employing FACS analysis and a microparticle analyzer we showed that erythrocyte cold storage indeed induces microparticle formation. We confirmed the pro-coagulant properties of these microparticles using a chromogenic substrate specific for thombin and a thrombin-anti-thrombin complex ELISA. To determine whether thrombin could induce adhesion of red blood cells to endothelial cells, we cultured human umbilical vein endothelial cells in micro-perfusion chambers and used live-imaging to define the adherence potential of the erythrocytes to endothelial cells at post-capillary flow rate. Thrombin stimulation of the endothelial cells did increase erythrocyte adhesion to endothelial cells. Moreover, the adhesion of erythrocytes followed a pattern resembling platelets binding to von Willebrand factor (VWF). By using live immunofluoresence imaging we confirmed that the erythrocytes did bind to VWF secreted from endothelial cells. Since erythrocyte-VWF interactions may be mediated by platelets, we used fluorescence cell sorting to remove platelets and erythrocyte-platelet complexes from erythrocyte concentrates. The purified erythrocytes did also bind to VWF secreted by endothelial cells and thereby we confirmed that erythrocytes can bind to VWF in a platelet-independent fashion. We further analyzed the specificity of the erythrocyte-VWF interaction by using different protein coatings in micro-perfusion chambers. Erythrocytes did bind to recombinant high molecular weight VWF multimers. Furthermore, they adhered more potently to VWF when compared to fibrinogen or fibrin but showed little binding to fibronectin, collagen type I, or subendothelial extra-cellular matrix proteins. Conclusion Our results suggest that transfusion of RBCs is able to induce endothelial binding of erythrocytes based on a VWF-erythrocyte interaction. We propose that passive infusion of cold stored erythrocyte derived microparticles promotes thrombin generation which subsequently activates endothelial cells and induces VWF secretion. This results in binding of red blood cells to endothelial cells in a platelet-independent fashion which requires the presence of VWF. Based on our results we hypothesize that binding of erythrocytes to VWF may occlude micro-capillaries thereby contributing to transfusion associated complications. Disclosures No relevant conflicts of interest to declare.
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Rivera, Alicia, Ana Ferreira, Danielle Bertoni, José R. Romero, and Carlo Brugnara. "Abnormal regulation of Mg2+ transport via Na/Mg exchanger in sickle erythrocytes." Blood 105, no. 1 (January 1, 2005): 382–86. http://dx.doi.org/10.1182/blood-2003-11-3755.
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Abstract Erythrocyte magnesium (Mg2+) deficiency has been demonstrated in sickle cell disease to contribute to erythrocyte dehydration, K loss, and thus sickling. No studies have assessed the functional properties of the Na/Mg exchanger in sickle cell disease. Using Mg2+-loaded erythrocytes, we measured Mg2+ efflux induced by extracellular Na+. We estimated that the Na/Mg exchanger had higher maximal velocity, higher affinity for Na+, and lower cooperativity for Mg2+ in sickle than in normal erythrocytes. The activity of the exchanger was markedly decreased by hypotonic and hypertonic conditions in normal erythrocytes but not in sickle erythrocytes. Studies of density-separated erythrocytes showed that the activity of the exchanger decreased as the mean cellular hemoglobin concentration increased in normal but not in sickle erythrocytes. Inhibition of protein kinase C (PKC) activity by calphostin C and chelerythrine increased the activity of the exchanger in normal but not in sickle erythrocytes. Inhibition of serine/threonine phosphatases did not affect the activity of the exchanger in either normal or sickle erythrocytes. Altogether, these data indicate that the Na/Mg exchanger is abnormally regulated in sickle erythrocytes. Therefore, Mg2+ depletion in sickle erythrocytes might be mediated by an up-regulated Na/Mg exchanger, possibly by dephosphorylation of the transporter or a closely associated regulator. (Blood. 2005;105:382-386)
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Alummoottil, Sajee, Mia J. van Rooy, Janette Bester, Craig Grobbelaar, and Alisa Phulukdaree. "Scanning Electron and Atomic Force Microscopic Analysis of Erythrocytes in a Cohort of Atopic Asthma Patients—A Pilot Study." Hemato 4, no. 1 (March 14, 2023): 90–99. http://dx.doi.org/10.3390/hemato4010009.
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Background: Non-communicable diseases are often associated with chronic inflammation, placing patients suffering from these conditions at a higher risk of thrombosis and other complications. The pathophysiology of asthma and/or atopic asthma is also linked to chronic inflammation, which consequently may alter blood parameters including erythrocyte structure and function. Methodology: The objective of this study was to evaluate differences in erythrocytes between patients with atopic asthma (n = 30) and healthy individuals (n = 30) by evaluating routine haematological parameters; structures and axial ratios of erythrocytes using light microscopy; erythrocyte membrane elasticity using atomic force microscopy; and erythrocyte ultrastructure using scanning electron microscopy. Results: The haematological findings of healthy participants and patients suffering from asthma were within normal clinical ranges together with significantly higher levels of circulating monocytes (p = 0.0066), erythrocytes (p = 0.0004), haemoglobin (p = 0.0057), and haematocrit (p = 0.0049) in asthma patients. The analysis of eosin-stained erythrocytes by light microscopy showed more echinocytes, acanthocytes, and ovalocytes compared to controls and a significant difference in axial ratios (p < 0.0001). Atomic force microscopy findings showed reduced erythrocyte membrane elasticity in asthmatic erythrocytes (p = 0.001). Ultrastructural differences in erythrocytes were visible in the asthma group compared to controls. Conclusion: Altered erythrocyte ultrastructural morphology and a significant change in the haematological profile are evident in atopic asthma and may influence common complications associated with asthma. The impact of these changes on the physiological mechanisms of coagulation and the pathophysiology of asthma needs to be further elucidated.
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Ideta, A., K. Tsuchiya, Y. Nakamura, M. Urakawa, M. Murakami, K. Hayama, and Y. Aoyagi. "277 EFFECTS OF ERYTHROCYTE AND ERYTHROCYTE HEMOLYSATE ON BOVINE PREIMPLANTATION EMBRYO DEVELOPMENT IN VITRO UNDER REACTIVE OXYGEN SPECIES CONDITION." Reproduction, Fertility and Development 22, no. 1 (2010): 295. http://dx.doi.org/10.1071/rdv22n1ab277.
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Reactive oxygen species (ROS) damage preimplantation embryos by increasing DNA fragmentation, leading to early embryonic death. Erythrocytes have been shown to protect other cells and tissues against ROS. In mice, erythrocytes were recently found to improve the early development of embryos by their antioxidant effect. The purpose of the present study was to examine the effect of erythrocytes on the in vitro development of bovine IVF embryos in medium supplemented with ROS. COCs were aspirated from ovaries collected from a local slaughterhouse and were cultured for 22 h in TCM-199 containing 5% fetal bovine serum. IVF was performed using an IVF100 (Research Institute for the Functional Peptides, Yamagata, Japan) according to the manufacturer’s instructions. In experiment 1, IVF embryos were cultured in CR1aa medium supplemented with an oxidizing agent, 0.5 mM hypoxanthine and 0.01 U mL-1 xanthine oxidase (HX/XOD), in the presence and absence of erythrocytes (5 × 104, 5× 105, 5×106, and 5 × 107 erythrocytes mL-1). In experiments 2 and 3, the development of embryos under the condition without ROS was assessed in the presence and absence of erythrocytes (5 × 106 erythrocytes mL-1) or erythrocyte hemolysate (hemoglobin concentration of 1.9 g L-1), respectively. At 7 days after in vitro culture, the development to the blastocyst stage of IVF embryos was examined using a stereomicroscope. Data were analyzed using Fisher’s PLSD test and Student’s t-test In experiment 1, the presence of HX/XOD significantly inhibited embryo development to the blastocyst stage in vitro (P < 0.05). The addition of erythrocytes to medium supplemented with HX/XOD markedly improved preimplantation development (Table 1). In experiments 2 and 3, supplementation of erythrocytes or erythrocyte hemolysate promoted the development of embryos to the blastocyst stage (experiment 2: erythrocyte 42.4 ± 3.1%, control 28.5 ± 5.7%, P < 0.1; experiment 3: erythrocyte hemolysate 39.1 ± 3.3%, control 30.2 ± 1.0%, P < 0.1). In conclusion, we suggest that the addition of erythrocytes to culture medium can counteract the negative effects of ROS on embryo development and blastocyst formation. Table 1.Effect of HX/XOD and erythrocyte supplementation on embryo development to blastocyst stage
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Jasenovec, Tomas, Dominika Radosinska, Katarina Jansakova, Maria Kopcikova, Aleksandra Tomova, Denisa Snurikova, Norbert Vrbjar, and Jana Radosinska. "Alterations in Antioxidant Status and Erythrocyte Properties in Children with Autism Spectrum Disorder." Antioxidants 12, no. 12 (November 28, 2023): 2054. http://dx.doi.org/10.3390/antiox12122054.
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Erythrocytes are responsible for the transport of oxygen within the organism, which is particularly important for nerve tissues. Erythrocyte quality has been shown to be deteriorated in oxidative stress conditions. In this study, we measured the same series of oxidative stress markers in plasma and erythrocytes to compare the differences between neurotypical children (controls) and children with autism spectrum disorder (ASD). We also focused on erythrocyte properties including their deformability, osmotic resistance, Na,K-ATPase activity, nitric oxide levels and free radical levels in children with ASD and controls. Greater oxidative damage to proteins and lipids was observed in the erythrocytes than in the plasma of ASD subjects. Additionally, antioxidant enzymes were more active in plasma samples from ASD children than in their erythrocytes. Significantly higher nitric oxide level and Na,K-ATPase enzyme activity were detected in erythrocytes of ASD individuals in comparison with the controls. Changes in oxidative status could at least partially contribute to the deterioration of erythrocyte morphology, as more frequent echinocyte formation was detected in ASD individuals. These alterations are most probably responsible for worsening the erythrocyte deformability observed in children with ASD. We can conclude that abnormalities in antioxidant status and erythrocyte properties could be involved in the pathomechanisms of ASD and eventually contribute to its clinical manifestations.
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Dwiyana, Yosepha, and Dalima AW Astrawinata. "PERUBAHAN BENTUK ERITROSIT DI GLOMERULONEFRITIS." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 20, no. 3 (October 16, 2016): 242. http://dx.doi.org/10.24293/ijcpml.v20i3.479.
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In glomerulonephritis there are intraglomerular inflammation, cell proliferation, and hematuria. Hematuria is characterized by more than 3 (three) erythrocytes per high-power field in the urine, which indicates the pathological processes in kidney or urinary tract. The combination of mechanical damage of erythrocyte membrane through the damaged glomerular basement membrane followed by the osmotic damage when it passes through the tubular system in the hypotonic osmotic solutions causes dysmorphic morphology. Erythrocytes trapped in the Tamm-Horsfall protein will form erythrocyte casts. Dysmorphic erythrocytes and or erythrocyte casts in the urine indicate glomerular hematuria. Various forms of dysmorphic erythrocytes in the urine can be found. Acanthocytes (G1-cells) are specific for glomerular hematury. The examination of these urinary sediments can be done natively or by using automated urinalysis analyzers.
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Al-kuraishy, Hayder M., Ali I. Al-Gareeb, Hope Onohuean, and Gaber El-Saber Batiha. "COVID-19 and erythrocrine function: The roller coaster and danger." International Journal of Immunopathology and Pharmacology 36 (January 2022): 039463202211031. http://dx.doi.org/10.1177/03946320221103151.
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Erythrocrine function refers to erythrocytes’ ability to synthesize and release active signaling molecules such as ATP and nitric oxide (NO). Erythrocyte NO regulates its deformability and increases its perfusion and circulation that prevent tissue hypoxia. Recently, there is a connotation between SARS-CoV-2 infection and erythrocrine function due to alteration in the release of NO and ATP from erythrocytes. SARS-CoV-2 binds erythrocyte band3 protein, which has a similar characteristic of ACE2, leading to alteration of erythrocyte physiology like oxygen transport with development of hypoxia. Similarly, SARS-CoV-2 infection activates erythrocyte protein kinase C alpha (PKC-α), causing significant changes in the erythrocyte functions. The erythrocytes can bind SARS-CoV-2 and its active particles with subsequent virus delivery to the liver and spleen macrophages. Thus, the erythrocytes act as elimination for SARS-CoV-2 in COVID-19. Moreover, the erythrocyte stored, release sphingosine-1 phosphate (S1P) improves endothelial and regulates lymphocyte functions. SARS-CoV-2 ORF8 protein binds the porphyrin part of hemoglobin heme at the β1 chain, causing hemolysis and dysfunctional hemoglobin to reduce oxygen-carrying capacity. In conclusion, SARS-CoV-2 infection and associated pro-inflammatory disorders lead to abnormal erythrocrine function with subsequent inflammatory complications and endothelial dysfunction due to deficiency of protective released molecules (NO, G1P, and ATP) from functional erythrocytes. In vitro, preclinical, and clinical studies are mandatory in this regard.
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Chen, Shao-Yin, Yulei Wang, Marilyn I. Telen, and Jen-Tsan A. Chi. "The Identification and Genomic Analysis of microRNAs in Human Erythrocytes in Sickle Cell Diseases." Blood 110, no. 11 (November 16, 2007): 3400. http://dx.doi.org/10.1182/blood.v110.11.3400.3400.
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Abstract Erythrocytes are circulating blood cells responsible for efficient gas exchange in human body. Since mature erythrocytes are terminally differentiated cells without nuclei and organelles, it is commonly thought that they do not contain nucleic acids. In this study, we re-examined this issue and found that human mature erythrocytes, while lacking ribosomal and large-sized RNAs, possess abundant small-sized RNAs. Using a combination of microarray analysis, real-time RT-PCR and Northern blots we found that mature erythrocytes contained abundant and diverse microRNAs which were distinct from microRNAs observed in reticulocytes/leukocytes and contributed to the majority of the microRNA expression in whole blood. When we used microarrays to analyze erythrocytes from normal (HbAA) and homozygous sickle (HbSS) individulas, we noted dramatic a difference in their microRNA expression pattern. To investigate how this difference is associated with erythrocyte disease phenotypes, we found that the poor expression of miR-320 was responsible for the defective downregulation of its target gene CD71 in HbSS cells during terminal differentiation. Collectively, we have discovered significant microRNA expression in human mature erythrocytes, which enables the microarray analysis of erythrocyte property to provide insights into the human erythrocyte diseases.
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Tutwiler, Valerie, Rustem I. Litvinov, Chandrasekaran Nagaswami, J. Eric Russell, Don L. Siegel, Carlos Hipolito Villa, Daniel Pan, Vladimir R. Muzykantov, and John W. Weisel. "Erythrocyte Rigidity Affects Blood Clot Contraction and Formation of Polyhedrocytes." Blood 128, no. 22 (December 2, 2016): 3814. http://dx.doi.org/10.1182/blood.v128.22.3814.3814.
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Abstract Blood clot contraction or retraction has been implicated to play a significant role in hemostasis, reduction of thrombus volume, and wound healing. Clot contraction is driven by forces that are generated by platelets and transmitted by fibrin and results in volume shrinkage followed by the compaction of erythrocytes into the core of the blood clot, resulting in their mechanical deformation towards a polyhedral shape, giving rise to the term polyhedrocytes. Despite the fact that erythrocytes are a major component of blood clots, relatively little is known about the influence of the mechanical properties or deformability of erythrocytes on the process of clot contraction. Increased hematocrit reduces extent of clot contraction due to mechanical resilience of erythrocytes and it is likely that in addition to a volume fraction the stiffness of erythrocytes can also affect the extent and rate of clot contraction. Here we tested this assumption by using artificially or naturally stiffened erythrocytes that have pathophysiological implications. The reduced deformability of erythrocytes is associated with a number of pathological conditions, such as hypertension, diabetes mellitus, atherosclerosis and smoking, but perhaps one of the most well-known diseases associated with increased erythrocyte rigidity is sickle cell disease (SCD). Another example of naturally stiff erythrocyte membrane is that of llama or camel that have red blood cells with increased osmotic resistance. To assess the extent of clot contraction, we used an optical tracking methodology that allows for the quantitative tracking for clot size. To assess the influence of erythrocyte rigidity on clot contraction we also used scanning electron microscopy to evaluate deformations of the erythrocytes, including the presence of polyhedrocytes. Centrifugation of citrated blood can be used to mimic the contractile forces generated by platelets and has been shown to cause polyhedrocyte formation. Increasing the erythrocyte rigidity through their treatment with a low concentration of glutaraldehyde resulted in a decrease in polyhedrocyte formation and the requirement of larger centrifugal forces to observe erythrocyte deformation, suggesting that the mechanical properties of erythrocytes could influence the process of clot contraction. As residual glutaraldehyde may have unwanted effects on platelets, clot contraction experiments were completed using naturally stiffer erythrocytes from SCD patients and llama ovalocytes, which are stiffer than human erythrocytes due to the increased amount of the membrane cytoskeletal protein spectrin. SCD patients were only included in this study if they had Sickle Trait, SCD Hb SS, SCD Hb SC and have not received recent transfusions. The blood samples of SCD patients were examined and on average had a 53% decrease (p<0.0001) in the extent of clot contraction compared to healthy subjects. Likewise, addition of llama ovalocytes to human platelet rich plasma resulted in a 28% decrease in extent of clot contraction compared to human erythrocytes and larger centrifugal forces were needed to see red cell deformation. SCD patients contracted 2.4X slower (p<0.001) during linear contraction (Phase 2) and 2.7X slower (p<0.05) during mechanical stabilization (Phase 3) when compared to healthy subjects. Clot contraction was impaired also by erythrocytes treated with antibodies that bind to the Wright b epitope on the erythrocytes and exert a rigidifying effect on the cells. The binding of the antibody to erythrocytes was determined by flow cytometry and the KD was ~50 nM. Increased red blood cell rigidity following exposure to antibodies was confirmed through mechanical and osmotic resistance and compared to unaltered erythrocytes. Collectively, these results demonstrate that erythrocyte mechanical properties can influence the process of clot contraction so that stiffer cells reduce the rate and extent of clot contraction. A better understanding of the role of erythrocyte deformability in the process of clot contraction has the potential to inform the development of more targeted treatments for limiting bleeding and thrombosis in patients who are prone to having altered erythrocyte content and mechanical properties of these highly abundant cells embedded into blood clots and thrombi. Disclosures Weisel: Bayer: Research Funding.