The influence of chlorpromazine on the potential-induced shape change of human erythrocyte

1991 ◽  
Vol 11 (4) ◽  
pp. 213-221 ◽  
Author(s):  
J. Hartmann ◽  
R. Glaser
Keyword(s):  
Red Blood Cells ◽  
Human Erythrocyte ◽  
Blood Cells ◽  
Characteristic Time ◽  
Time Course ◽  
Transmembrane Potential ◽  
Shape Change ◽  
Human Erythrocytes

The effect of chlorpromazine (CPZ) on the shape of human erythrocytes with different values of transmembrane potential (TMP) was investigated. The shape of red blood cells with negative values of the TMP remained unchanged after the formation of stomatocytes by chlorpromazine, while cells with positive TMP showed a characteristic time course of shape change during the incubation with CPZ. Experiments with vanadate show that this might be due to a difference in the activity of the phospholipid-translocase at different values of TMP.

scholarly journals Studies of Human Erythrocyte Catalase by Fluorescent Antibody Technic The Distribution of Catalase in Acatalasia and Hypocatalasia

Blood ◽  
1969 ◽  
Vol 34 (1) ◽  
pp. 25-31
Author(s):  
TAKEMITSU HOSOI ◽  
SEIJI YAHARA ◽  
HOWARD B. HAMILTON ◽  
NORIO FUJIKI ◽  
TERUO SASAKI ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Human Erythrocyte ◽  
Blood Cells ◽  
Fluorescent Antibody ◽  
Double Diffusion ◽  
Human Erythrocytes ◽  
Red Cells ◽  
Diffusion Method ◽  
Cellular Distribution ◽  
Erythrocyte Catalase

Abstract In order to investigate the cellular distribution of catalase in normal, hypocatalasic and acatalasic red blood cells, the fluorescent antibody labelling technic was employed. Sensitive anticatalase sera were produced in rabbits by immunization with purified catalase extracted from human erythrocytes. Specificity against human erythrocyte catalase was confirmed by Ouchterlony’s double diffusion method. The distribution of catalase is fairly homogeneous in normal and hypocatalasic red cells, but in acatalasic cells fluorescence due to the presence of catalase was not observed. By this method the amount of catalase in hypocatalasic red cells was judged to be between that of normal and acatalasic red cells.

scholarly journals FUSION OF INTACT HUMAN ERYTHROCYTES AND ERYTHROCYTE GHOSTS

1974 ◽  
Vol 63 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Hava Peretz ◽  
Zivia Toister ◽  
Yehudith Laster ◽  
Abraham Loyter
Keyword(s):  
Red Blood Cells ◽  
Clostridium Perfringens ◽  
Human Erythrocyte ◽  
Blood Cells ◽  
Sendai Virus ◽  
Iodoacetic Acid ◽  
Human Erythrocytes ◽  
Erythrocyte Ghosts ◽  
Human Red Blood Cells ◽  
Bivalent Cations

Sendai virus is able to induce the fusion of human erythrocytes. Bivalent cations or ATP are not essential for polyerythrocyte formation. High fusion indices were obtained when Sendai virus was added to cells incubated in the presence of both EDTA and iodoacetic acid. Human erythrocyte ghosts prepared by gradual hemolysis still retain the potential to undergo virus-induced fusion. Fusion of human red blood cells without the addition of viruses was obtained by incubation of erythrocytes at pH 10.5 in the presence of Ca++ (40 mM) or by addition of phospholipase C Clostridium perfringens preparations to cells previously agglutinated or polylysine.

scholarly journals Dielectric characterization of Plasmodium falciparum -infected red blood cells using microfluidic impedance cytometry

2018 ◽  
Vol 15 (147) ◽  
pp. 20180416 ◽  
Author(s):  
C. Honrado ◽  
L. Ciuffreda ◽  
D. Spencer ◽  
L. Ranford-Cartwright ◽  
H. Morgan
Keyword(s):  
Plasmodium Falciparum ◽  
Dielectric Properties ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Time Course ◽  
Fluorescent Protein ◽  
Clear Understanding ◽  
Infection Cycle ◽  
Dielectric Characterization ◽  
Impedance Cytometry

Although malaria is the world's most life-threatening parasitic disease, there is no clear understanding of how certain biophysical properties of infected cells change during the malaria infection cycle. In this article, we use microfluidic impedance cytometry to measure the dielectric properties of Plasmodium falciparum -infected red blood cells ( i- RBCs) at specific time points during the infection cycle. Individual parasites were identified within i- RBCs using green fluorescent protein (GFP) emission. The dielectric properties of cell sub-populations were determined using the multi-shell model. Analysis showed that the membrane capacitance and cytoplasmic conductivity of i- RBCs increased along the infection time course, due to membrane alterations caused by parasite infection. The volume ratio occupied by the parasite was estimated to vary from less than 10% at earlier stages, to approximately 90% at later stages. This knowledge could be used to develop new label-free cell sorting techniques for sample pre-enrichment, improving diagnosis.

scholarly journals PIEZO1 and the mechanism of the long circulatory longevity of human red blood cells

2021 ◽  
Vol 17 (3) ◽  
pp. e1008496
Author(s):  
Simon Rogers ◽  
Virgilio L. Lew
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Time Course ◽  
Clinical Manifestations ◽  
Cell Subpopulation ◽  
Unexpected Finding ◽  
Human Red Blood Cells ◽  
Acceptable Model ◽  
New Finding ◽  
Extended Longevity

Human red blood cells (RBCs) have a circulatory lifespan of about four months. Under constant oxidative and mechanical stress, but devoid of organelles and deprived of biosynthetic capacity for protein renewal, RBCs undergo substantial homeostatic changes, progressive densification followed by late density reversal among others, changes assumed to have been harnessed by evolution to sustain the rheological competence of the RBCs for as long as possible. The unknown mechanisms by which this is achieved are the subject of this investigation. Each RBC traverses capillaries between 1000 and 2000 times per day, roughly one transit per minute. A dedicated Lifespan model of RBC homeostasis was developed as an extension of the RCM introduced in the previous paper to explore the cumulative patterns predicted for repetitive capillary transits over a standardized lifespan period of 120 days, using experimental data to constrain the range of acceptable model outcomes. Capillary transits were simulated by periods of elevated cell/medium volume ratios and by transient deformation-induced permeability changes attributed to PIEZO1 channel mediation as outlined in the previous paper. The first unexpected finding was that quantal density changes generated during single capillary transits cease accumulating after a few days and cannot account for the observed progressive densification of RBCs on their own, thus ruling out the quantal hypothesis. The second unexpected finding was that the documented patterns of RBC densification and late reversal could only be emulated by the implementation of a strict time-course of decay in the activities of the calcium and Na/K pumps, suggestive of a selective mechanism enabling the extended longevity of RBCs. The densification pattern over most of the circulatory lifespan was determined by calcium pump decay whereas late density reversal was shaped by the pattern of Na/K pump decay. A third finding was that both quantal changes and pump-decay regimes were necessary to account for the documented lifespan pattern, neither sufficient on their own. A fourth new finding revealed that RBCs exposed to levels of PIEZO1-medited calcium permeation above certain thresholds in the circulation could develop a pattern of early or late hyperdense collapse followed by delayed density reversal. When tested over much reduced lifespan periods the results reproduced the known circulatory fate of irreversible sickle cells, the cell subpopulation responsible for vaso-occlusion and for most of the clinical manifestations of sickle cell disease. Analysis of the results provided an insightful new understanding of the mechanisms driving the changes in RBC homeostasis during circulatory aging in health and disease.

Cell volume and metabolic dependence of NEM-activated K+-Cl- flux in human red blood cells

1985 ◽  
Vol 249 (1) ◽  
pp. C124-C128 ◽  
Author(s):  
P. K. Lauf ◽  
C. M. Perkins ◽  
N. C. Adragna
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Blood Cells ◽  
Time Course ◽  
Transport Activity ◽  
Human Red Blood Cells ◽  
Atp Breakdown ◽  
The Difference ◽  
Metabolic Dependence ◽  
K Transport

The effects of incubation in anisosmotic media and of metabolic depletion on ouabain-resistant (OR) Cl--dependent K+ influxes stimulated by N-ethylmaleimide (NEM) were studied in human red blood cells using Rb+ as K+ analogue. The NEM-stimulated but not the basal Rb+-Cl- influx measured in phosphate-buffered anisosmotic media was found to be cell volume dependent. When cellular ATP, [ATP]c, was lowered to less than 0.10 of its initial level by exposure to nonmetabolizable 2-deoxy-D-glucose, the NEM-stimulated but not the basal Cl--dependent Rb+ influxes were abolished. Metabolically depleted red blood cells subsequently repleted by incubation in glucose plus inosine regained the NEM-inducible Rb+ (K+) transport activity. The difference in the time course of ATP breakdown and Rb+ influx inhibition suggests that energization of the NEM-stimulated Rb+ flux by metabolism may involve factors additional to ATP.

scholarly journals Morphological Sequence of Spontaneously Forming Parietal Thrombi as Observed by Scanning Electron Microscopy (SEM)

1977 ◽  
Author(s):  
H.J. Genz ◽  
H. Metzger ◽  
P.F. Tauber ◽  
H. Ludwig
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Shape Change ◽  
Inhibitory Effect ◽  
Endothelial Surface ◽  
Morphological Criteria ◽  
Fibrin Network ◽  
Tissue Specimens ◽  
Cellular Control

Spontaneous thrombus formation in human mesenteric veins was studied with the SEM. Tissue specimens were prepared according to Ludwig et al., Acta anatomica, 96, 469-477(1976). Platelet shape change, thrombus formation and organization and the morphological interactions between the various corpuscular elements of blood are demonstrated. The following morphological criteria of these processes are observed :(1) Platelets adhere to distinctly altered endothelial surfaces and exhibit pores in the membrane and pseudopodia. (2) Platelet aggregation and thrombus formation occur next to each other along the endothelial surface. Thrombi contain red blood cells and also a larger number of lymphocytes, but only a few platelets are hold prisoners within the fibrin network. Once caught in the mesh, such platelets do not show shape change compared to those being in contact with the endothelium. (3) Red blood cells between the thrombus fibers undergo form changes. Lymphocytes remain unaltered, but vice versa destroy adjacent fibrin fibers leading to partial loss of thrombus stability. This destruction occurs to a much lesser degree when platelets are near to the lymphocytes. It seems conceivable that platelets exert an inhibitory effect towards lymphocyte-induced fibrin proteolysis. The data suggest that both platelets and lymphocytes possibly represent a cellular control system that is responsible for the physiological clearance of spontaneously formed thrombi.

Shortened Lifespan of Red Blood Cells and the Effects of Erythropoietin in Rats with Nephrogenic Anemia.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1977-1977
Author(s):  
Yoshiyuki Iwatsuki ◽  
Koki Kitamura ◽  
Ken-ichi Suzuki
Keyword(s):  
Red Blood Cells ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Time Course ◽  
Annexin V ◽  
Renal Anemia ◽  
Normal Donor ◽  
Human Erythropoietin ◽  
Male Wistar Rats ◽  
Rbc Count

Abstract Abstract 1977 Poster Board I-1000 Anemia is a common complication of chronic kidney disease (CKD), mainly due to the inability of the kidneys to secrete enough erythropoietin to adequately stimulate hematopoiesis. Further, given that the lifespan of red blood cells (RBCs) has been reported to be reduced in CKD patients, this reduction in RBC lifespan is believed to be a part of the etiology of renal anemia. In the present study, we focused on RBC survival and measured the lifespan of RBCs in rats with nephrogenic anemia. We also examined the effects of erythropoietin on RBC lifespan in this anemia model. Nephrogenic anemia was induced by oral administration of adenine (600 mg/kg/day for 10 days) to male Wistar rats. Progressive, serious anemia associated with increased levels of plasma creatinine was observed in the rats. On Day 40, the number of RBCs and hemoglobin (HGB) levels were lower in the adenine-treated rats than in normal, control rats (normal: 930×104/μL, anemic: 677×104/μL for RBC and normal: 17.2 g/dL, anemic: 13.4 g/dL for HGB). However, the number of reticulocytes did not change in the anemic rats (normal: 299×103/μL, anemic: 329×103/μL, P = 0.102). The percentage of annexin V-binding erythrocytes was increased in anemic rats (normal: 0.77%, anemic 1.76%) and inversely correlated with RBC count and HGB levels, suggesting that apoptosis of RBCs increased as anemia progressed. Taking these findings into account, we measured the lifespan of RBCs in rats with nephrogenic anemia. We transfused 5-chloromethylfluorescein diacetate (CMFDA)-labeled RBCs from normal donor rats into either normal or anemic recipients and determined the number of labeled RBCs present in the peripheral blood at various time points thereafter. The time course of the reduction in the percentage of labeled RBCs in peripheral blood revealed that the half-life (t1/2) of RBCs in anemic rats was shorter than in normal rats (normal: 22.5 d, anemic: 13.3 d). This reduction in RBC lifespan was also observed in a rat model of cisplatin-induced renal anemia. Injection of anemic rats with recombinant human erythropoietin (rhEPO) restored the number of RBCs and HGB concentration to normal levels. However, the t1/2of RBCs in these rats was not changed. The clearance of RBCs in anemic rats does not appear to be influenced by rhEPO injection. In conclusion, the survival of RBCs was reduced in rats with nephrogenic anemia, an observation consistent with the shortened survival time of RBCs in renal failure patients. This finding suggests that this model is suitable for investigating drugs which may be used in the treatment of renal anemia. Further, because EPO therapy did not affect the lifespan of RBCs, agents which improve the shortened RBC survival inherent in CKD patients may be useful in treating renal anemia. Disclosures: Iwatsuki: Astellas Pharma Inc.: Employment. Kitamura:Astellas Research Institute of America LLC: Employment. Suzuki:Astellas Pharma Inc.: Employment.

Forssman expression on human erythrocytes: biochemical and genetic evidence of a new histo-blood group system

Blood ◽  
2013 ◽  
Vol 121 (8) ◽  
pp. 1459-1468 ◽  
Author(s):  
Lola Svensson ◽  
Annika K. Hult ◽  
Robert Stamps ◽  
Jonas Ångström ◽  
Susann Teneberg ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Group ◽  
Blood Cells ◽  
Human Erythrocytes ◽  
Blood Group System ◽  
Group System ◽  
Glycolipid Antigen ◽  
Human Red Blood Cells ◽  
Key Points ◽  
Forssman Antigen

Key Points A new histo-blood group system was discovered, based on the identification of Forssman glycolipid antigen on human red blood cells. A newly described polymorphism in the GBGT1 gene activates the encoded enzyme to synthesize Forssman antigen.

scholarly journals The circulatory physiopathology of human red blood cells investigated with a multiplatform model of cellular homeostasis. III. Senescence changes during the full circulatory lifespan

2020 ◽  
Author(s):  
Simon Rogers ◽  
Virgilio L. Lew
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Time Course ◽  
Clinical Manifestations ◽  
Cell Subpopulation ◽  
Unexpected Finding ◽  
Sickle Cells ◽  
Human Red Blood Cells ◽  
Decay Sequence ◽  
Health And Disease

AbstractHuman red blood cells (RBCs) have a circulatory lifespan of about four months. Under constant oxidative and mechanical stress, but devoid of organelles and deprived of biosynthetic capacity for protein renewal, RBCs undergo substantial homeostatic changes, progressive densification followed by late density reversal among others, changes assumed to have been harnessed by evolution to sustain the rheological competence of the RBCs for as long as possible. The unknown mechanisms by which this is achieved are the subject of this investigation. Each RBC traverses capillaries between 1000 and 2000 times per day, roughly one transit per minute, a total of about 2•105 transits during their lifespan. A dedicated Lifespan model of RBC homeostasis was developed as an extension of the RCM introduced in the first paper of this series to explore the cumulative patterns predicted for repetitive capillary transits over a standardized lifespan period of 120 days, using experimental data to constrain the parameter space. Capillary transits were simulated by periods of elevated cell/medium volume ratios and by transient deformation-induced permeability changes attributed to PIEZO1 channel mediation as outlined in the second paper of this series. The first unexpected finding was that quantal changes generated during single capillary transits cease accumulating after a few days and cannot account for the observed progressive densification of RBCs on their own, thus ruling out the quantal hypothesis. The second unexpected finding was that the documented patterns of RBC densification and late reversal could only be emulated by the implementation of a strict time-course of decay in the activities of the calcium and Na/K pumps, but only in addition to the quantal changes. These results showed that both quantal changes and pump-decay regimes were necessary to account for the documented lifespan pattern, neither sufficient on their own. They also suggested a strong selective component in the pump decay sequence. A third finding was that RBCs exposed to levels of calcium permeation above certain thresholds in the circulation could develop a pattern of late or early hyperdense collapse followed by delayed density reversal. When tested over much reduced lifespan periods the results emulated the known circulatory fate of irreversible sickle cells, the cell subpopulation responsible for vaso-occlusion and for most of the clinical manifestations of sickle cell disease. Analysis of the results provided an insightful new understanding of the mechanisms driving the changes in RBC homeostasis during circulatory aging in health and disease.

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