Iron absorption in hypotransferrinemic mice [see comments]

Abstract We used a unique animal model, the hypotransferrinemic (Htx) mouse, to examine the role of transferrin (Tf) in gastrointestinal iron uptake. Despite the absence of Tf, Htx animals hyperabsorb iron. Transfusion of red blood cells sufficient to normalize the hematocrit and reticulocyte count resulted in a return of iron absorption to normal values. These studies indicate that Tf does not play an obligate role in iron absorption, either as a carrier or as a humoral signal regulating absorption. Transfer of plasma or whole blood from Htx mice or from other animal models of iron hyperabsorption to normal mice did not cause an increase in iron absorption in recipient animals. Using the plasma or blood transfer approach, we have been unable to detect a humoral regulator of gastrointestinal iron absorption.

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Iron absorption in hypotransferrinemic mice [see comments]

Blood ◽

10.1182/blood.v78.12.3288.bloodjournal78123288 ◽

1991 ◽

Vol 78 (12) ◽

pp. 3288-3290 ◽

Cited By ~ 1

Author(s):

SS Buys ◽

CB Martin ◽

M Eldridge ◽

JP Kushner ◽

J Kaplan

Keyword(s):

Animal Model ◽

Animal Models ◽

Red Blood Cells ◽

Whole Blood ◽

Blood Cells ◽

Iron Uptake ◽

Iron Absorption ◽

Normal Values ◽

Reticulocyte Count

We used a unique animal model, the hypotransferrinemic (Htx) mouse, to examine the role of transferrin (Tf) in gastrointestinal iron uptake. Despite the absence of Tf, Htx animals hyperabsorb iron. Transfusion of red blood cells sufficient to normalize the hematocrit and reticulocyte count resulted in a return of iron absorption to normal values. These studies indicate that Tf does not play an obligate role in iron absorption, either as a carrier or as a humoral signal regulating absorption. Transfer of plasma or whole blood from Htx mice or from other animal models of iron hyperabsorption to normal mice did not cause an increase in iron absorption in recipient animals. Using the plasma or blood transfer approach, we have been unable to detect a humoral regulator of gastrointestinal iron absorption.

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The role of red blood cells in platelet aggregation in whole blood

Atherosclerosis ◽

10.1016/0021-9150(88)90151-7 ◽

1988 ◽

Vol 71 (2-3) ◽

pp. 261-262 ◽

Cited By ~ 6

Author(s):

P. Brown ◽

M.J.G. Harrison

Keyword(s):

Platelet Aggregation ◽

Red Blood Cells ◽

Whole Blood ◽

Blood Cells

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The Role Of Red Blood Cells In Spontaneous Aggregation Of Platelets In Whole Blood

Biomaterials in Artificial Organs ◽

10.1007/978-1-349-07283-5_33 ◽

1984 ◽

pp. 249-257 ◽

Cited By ~ 1

Author(s):

A. R. Saniabadi ◽

G. D. O. Lowe ◽

C. D. Forbes ◽

C. R. M. Prentice ◽

J. C. Barbenel

Keyword(s):

Red Blood Cells ◽

Whole Blood ◽

Blood Cells ◽

Spontaneous Aggregation ◽

Aggregation Of Platelets

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Role of erythrocyte in regulating local O2delivery mediated by hemoglobin oxygenation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.280.6.h2833 ◽

2001 ◽

Vol 280 (6) ◽

pp. H2833-H2839 ◽

Cited By ~ 129

Author(s):

Justin E. Jagger ◽

Ryon M. Bateman ◽

Mary L. Ellsworth ◽

Chris G. Ellis

Keyword(s):

Red Blood Cells ◽

Whole Blood ◽

Blood Cells ◽

Membrane Surface ◽

Atp Production ◽

Fluoride Treatment ◽

Hemoglobin Molecule ◽

Hemoglobin Oxygenation

The release of ATP from red blood cells (RBC) in response to low O2 levels is linked to ATP production and the oxygenation state of hemoglobin. Because O2 is unloaded from the RBC, the concentration of deoxygenated hemoglobin increases, displacing phosphofructokinase from the cytoplasmic domain of band 3. We hypothesize that the ATP molecules produced through this glycolytic stimulation at the membrane surface result in the release of ATP from the RBC. Rat whole blood exposed to 5 min of low Po 2 in vitro increased plasma [ATP] by 1.0 μM (+45%). This increase was reduced to 0.1 μM (+12%, P < 0.05) after citrate incubation and reversed after fluoride treatment (both glycolytic inhibitors) by −0.2 μM (−23%, P < 0.05). Plasma [ATP] of control RBC decreased −0.3 μM (−12%) when 8% CO ( P < 0.05) was added to the chamber. Because CO and O2 bind competitively to heme, these results support our hypothesis that the release of ATP from RBC is linked to ATP production through the oxygenation state of the hemoglobin molecule.

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Reactivity and Speciation of Anti-Diabetic Vanadium Complexes in Whole Blood and Its Components: The Important Role of Red Blood Cells

Inorganic Chemistry ◽

10.1021/acs.inorgchem.5b00665 ◽

2015 ◽

Vol 54 (16) ◽

pp. 7753-7766 ◽

Cited By ~ 50

Author(s):

Aviva Levina ◽

Andrew I. McLeod ◽

Sylvia J. Gasparini ◽

Annie Nguyen ◽

W. G. Manori De Silva ◽

...

Keyword(s):

Red Blood Cells ◽

Whole Blood ◽

Blood Cells ◽

Vanadium Complexes

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An Evaluation of Morphological Changes and Deformability of Suspended Red Blood Cells Prepared Using Whole Blood with Different Hemoglobin Levels of Tibetans

Transfusion Medicine and Hemotherapy ◽

10.1159/000513319 ◽

2021 ◽

pp. 1-10

Author(s):

Rui Zhong ◽

Dingding Han ◽

Xiaodong Wu ◽

Hong Wang ◽

Wanjing Li ◽

...

Keyword(s):

Red Blood Cells ◽

Whole Blood ◽

Blood Cells ◽

Morphological Changes ◽

Osmotic Fragility ◽

Spherical Shape ◽

Hypoxic Environment ◽

Wide Range ◽

Group A ◽

Cell Membrane Protein

Background: The hypoxic environment stimulates the human body to increase the levels of hemoglobin (HGB) and hematocrit and the number of red blood cells. Such enhancements have individual differences, leading to a wide range of HGB in Tibetans’ whole blood (WB). Study Design: WB of male Tibetans was divided into 3 groups according to different HGB (i.e., A: >120 but ≤185 g/L, B: >185 but ≤210 g/L, and C: >210 g/L). Suspended red blood cells (SRBC) processed by collected WB and stored in standard conditions were examined aseptically on days 1, 14, 21, and 35 after storage. The routine biochemical indexes, deformability, cell morphology, and membrane proteins were tested. Results: Mean corpuscular volume, adenosine triphosphate, pH, and deformability were not different in group A vs. those in storage (p > 0.05). The increased rate of irreversible morphology of red blood cells was different among the 3 groups, but there was no difference in the percentage of red blood cells with an irreversible morphology after 35 days of storage. Group C performed better in terms of osmotic fragility and showed a lower rigid index than group A. Furthermore, SDS-PAGE revealed similar cross-linking degrees of cell membrane protein but the band 3 protein of group C seemed to experience weaker clustering than that of group A as detected by Western Blot analysis after 35 days of storage. Conclusions: There was no difference in deformability or morphological changes in the 3 groups over the 35 days of storage. High HGB levels of plateau SRBC did not accelerate the RBC change from a biconcave disc into a spherical shape and it did not cause a reduction in deformability during 35 days of preservation in bank conditions.

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Glycophorin A-based exclusion of red blood cells for flow cytometric analysis of platelet glycoprotein expression in citrated whole blood

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2020-0014 ◽

2020 ◽

Vol 0 (0) ◽

Author(s):

Christina Berens ◽

Johannes Oldenburg ◽

Bernd Pötzsch ◽

Jens Müller

Keyword(s):

Red Blood Cells ◽

Expression Analysis ◽

Whole Blood ◽

Blood Cells ◽

Control Sample ◽

Small Sample ◽

Platelet Glycoprotein ◽

Glycophorin A ◽

Giant Platelets ◽

Platelet Counts

AbstractObjectivesAnalysis of platelet glycoprotein (GP) expression by flow cytometry is applied for diagnostic confirmation of GP-associated thrombocytopathies. While platelet-rich plasma may be used for distinct identification of target events, this strategy is not feasible for small sample volumes or for patients showing low platelet counts and/or giant platelets. However, also the use of whole blood (WB) is hampered by the difficulty to discriminate platelets from red blood cells (RBC) in such patients. To circumvent these limitations, we evaluated the feasibility of a RBC gating-out strategy.MethodsIn addition to platelet GPIb, GPIIa/IIIa, as well as P-selectin (CD62P), citrated whole blood (CWB) samples were stained for RBC-specific glycophorin A (CD235a). CD235a-negative platelet events were further discriminated by forward-/side-scatter characteristics and platelet GP expressions analyzed relative to that of a healthy control sample processed in parallel.ResultsEstablished reference intervals allowed for clear identification of decreased GPIIb/IIIa- or GPIb expression pattern in samples of patients with confirmed Glanzmann thrombasthenia or Bernard–Soulier syndrome, respectively. It could be shown that the analysis of 2,500 platelet events is sufficient for reliable GP expression analysis, rendering the proposed method applicable to samples with low platelet counts.ConclusionsThis study demonstrates the feasibility of CD235a-based exclusion of RBC for platelet GP expression analysis in CWB. In contrast to direct staining of platelet-specific antigens for target identification, this indirect gating out approach is generally applicable independent of any underlying platelet GP expression deficiency.

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Role of Adhesion Molecules and Vascular Endothelium in the Pathogenesis of Sickle Cell Disease

Hematology ◽

10.1182/asheducation-2007.1.84 ◽

2007 ◽

Vol 2007 (1) ◽

pp. 84-90 ◽

Cited By ~ 27

Author(s):

Marilyn J. Telen

Keyword(s):

Sickle Cell Disease ◽

Red Blood Cells ◽

Adhesion Molecules ◽

Sickle Cell ◽

Vascular Endothelium ◽

Blood Cells ◽

Cell Disease ◽

Adhesive Interactions ◽

Lines Of Evidence

AbstractA number of lines of evidence now support the hypothesis that vaso-occlusion and several of the sequelae of sickle cell disease (SCD) arise, at least in part, from adhesive interactions of sickle red blood cells, leukocytes, and the endothelium. Both experimental and genetic evidence provide support for the importance of these interactions. It is likely that future therapies for SCD might target one or more of these interactions.

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Role of Calcium in Phosphatidylserine Externalisation in Red Blood Cells from Sickle Cell Patients

Anemia ◽

10.1155/2011/379894 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 11

Author(s):

Erwin Weiss ◽

David Charles Rees ◽

John Stanley Gibson

Keyword(s):

Red Blood Cells ◽

Sickle Cell ◽

Blood Cells ◽

Phosphatidylserine Exposure ◽

Channel Inhibition ◽

Cation Conductance ◽

Gardos Channel ◽

Cation Permeability

Phosphatidylserine exposure occurs in red blood cells (RBCs) from sickle cell disease (SCD) patients and is increased by deoxygenation. The mechanisms responsible remain unclear. RBCs from SCD patients also have elevated cation permeability, and, in particular, a deoxygenation-induced cation conductance which mediates entry, providing an obvious link with phosphatidylserine exposure. The role of was investigated using FITC-labelled annexin. Results confirmed high phosphatidylserine exposure in RBCs from SCD patients increasing upon deoxygenation. When deoxygenated, phosphatidylserine exposure was further elevated as extracellular [] was increased. This effect was inhibited by dipyridamole, intracellular chelation, and Gardos channel inhibition. Phosphatidylserine exposure was reduced in high saline. levels required to elicit phosphatidylserine exposure were in the low micromolar range. Findings are consistent with entry through the deoxygenation-induced pathway (), activating the Gardos channel. [] required for phosphatidylserine scrambling are in the range achievablein vivo.

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