Vesicles generated during storage of red cells are rich in the lipid raft marker stomatin

Salzer, Ulrich; Zhu, Rong; Luten, Marleen; Pastushenko, V. F.; Perkmann, Thomas; Hinterdorfer, Peter; Bosman, G.J.C.G.M.

doi:10.1111/j.1537-2995.2007.01549.x

Cited by 141 publications

(165 citation statements)

References 68 publications

(88 reference statements)

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“…Forwardand sideward-scatter analysis revealed a homogenous population that was >95% positive for Ter119, indicating their RBC origin. Consistent with previous reports in humans, 20 between 25% and 45% of all microvesicles stained positive for annexin V, indicating surface expression of PS ( Figure 1A). Electron microscopy revealed round-shaped vesicles with a size ≈200 nm ( Figure 1B), a finding that was confirmed by nanoparticle tracking analysis ( Figure 1C).…”

Section: Characterization Of Rbc-mvsupporting

confidence: 80%

Erythrocyte-Derived Microvesicles Amplify Systemic Inflammation by Thrombin-Dependent Activation of Complement

Zecher

Čumpelik

Schifferli

2014

ATVB

108

100

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Objective-Transfusion of aged blood has been associated with increased morbidity and mortality in critically ill patients.During storage, erythrocytes release increasing numbers of microvesicles (red blood cell-derived microvesicles [RBC-MV]). We hypothesized that RBC-MV mediate some of the deleterious effects of aged blood transfusions. Approach and Results-We established a murine transfusion model using RBC-MV purified from aged mouse erythrocytes. Injection of RBC-MV into healthy mice had no effect. However, they aggravated pulmonary leukocyte sequestration and peripheral blood leukopenia induced by lipopolysaccharides. Lipopolysaccharide-induced proinflammatory cytokines were significantly increased in plasma after RBC-MV injection. These effects were not seen in C5aR-deficient mice. In vitro, RBC-MV bound C3 fragments after incubation with plasma but failed to bind immunoglobulins, C1q, or mannose-binding lectin. Preventing thrombin generation inhibited complement activation in vitro and in vivo and reversed the proinflammatory effects of RBC-MV in lipopolysaccharide-primed mice. Finally, the RBC-MV-induced phenotype was recapitulated using phosphatidylserineexpressing liposomes, suggesting that surface expression of phosphatidylserine by RBC-MV was mechanistically involved. Conclusions-These

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Section: Characterization Of Rbc-mvsupporting

confidence: 80%

Erythrocyte-Derived Microvesicles Amplify Systemic Inflammation by Thrombin-Dependent Activation of Complement

Zecher

Čumpelik

Schifferli

2014

ATVB

108

100

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“…23 The other newly identified components, flotillins and stomatin, belong to distinct erythrocyte lipid rafts. 24,25 Some of these cytoskeletonassociated proteins might be interconnected rather than directly binding to AE1. The mass spectrometry (MS)-identified proteins were validated by immunoblot analysis (Figure 2).…”

Section: Resultsmentioning

confidence: 99%

Miltenberger blood group antigen type III (Mi.III) enhances the expression of band 3

Hsu

Chi

Guček

et al. 2009

Blood

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The special blood group antigen Mi.III exhibits a characteristic hybrid structure of glycophorin A (GPA) and glycophorin B, termed Gp.Mur. This phenotype has exceptionally high occurrence rates in several indigenous tribes in Taiwan (ϳ21.2%-88.4%). Because glycophorin/ Miltenberger begins interaction with anion exchanger-1 (AE1) in the endoplasmic reticulum, we hypothesized that the AE1-based macrocomplexes on erythrocyte membranes obtained from Mi.III ؉ people could be differentiated from those obtained from non-Miltenberger people. Quantitative mass spectrometric comparison of the AE1-based complexes by iTRAQ™ (Applied Biosystems) revealed 25% to 67% higher expression of AE1 in Mi.III ؉ erythrocytes. In accordance with the higher AE1 level, the Mi.III ؉ erythrocytes exhibited superior HCO 3 ؊ capacities, pH homeostasis, and osmotic resistance. Cotransfection experiments in HEK293 cells showed that Gp.Mur, like GPA, enhanced trafficking of AE1 to the plasma membrane. In summary, the increased surface expression of AE1 in Mi.III ؉ erythrocytes could be attributed to the additive effect of GPA and Gp

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“…While we do not have enough evidence to firmly defend this hypothesis, current knowledge does support its feasibility. First, glycosphingolipids, a minor component of membrane lipids, are found in lipid rafts (39) that are present in RBCs (40) and are implicated in the modification of RBC shape (41). Second, the lipid composition of microdomains is altered in a macrophagic model of Gaucher cells (42).…”

Section: Discussionmentioning

confidence: 99%

A cytometric study of the red blood cells in Gaucher disease reveals their abnormal shape that may be involved in increased erythrophagocytosis

Bratosin

Tissier²,

Lapillonne

et al. 2010

Cytometry

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Background: Gaucher disease is a sphingolipidosis caused by a deficiency of the enzyme glucocerebrosidase. Macrophages transform into pathogenic Gaucher cells following the phagocytosis of red blood cells (RBCs) and subsequent accumulation of glucosylceramide. Enhanced erythrophagocytosis is one feature of the disease indicating abnormal macrophage-RBC interactions. We hypothesized that the erythrophagocytosis observed in Gaucher disease may be at least partly due to abnormalities in the RBCs themselves.Methods: To investigate this hypothesis, we used flow cytometry FSC/SSC to study RBCs sampled from seven patients with Gaucher disease in terms of their shape and the expression of markers of senescence and phagocytosis. Cells from two of the seven patients were evaluated before and 9 months after the start of enzyme-replacement therapy.Results: Untreated patients were found to have abnormal flow-cytometry profiles suggesting an alteration of Gaucher RBC morphology. Scanning electron microscopy confirmed this finding by revealing many abnormally shaped RBCs. Whereas there was no evidence of desialylation of membrane glycoconjugates or phosphatidylserine exposure, RBC viability (calcein-AM test) and CD47 expression were reduced. These anomalies found in RBCs sampled from two patients before treatment, were no longer present after a 9 month-long enzyme-replacement therapy.Conclusions: We report on previously overlooked alterations of Gaucher RBCs that may facilitate erythrophagocytosis in untreated patients. Their potential role in the anemia, the excess of aggregation and rheological anomalies associated with Gaucher disease must now be addressed. RBC anomalies may

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Vesicles generated during storage of red cells are rich in the lipid raft marker stomatin

Cited by 141 publications

References 68 publications

Erythrocyte-Derived Microvesicles Amplify Systemic Inflammation by Thrombin-Dependent Activation of Complement

Erythrocyte-Derived Microvesicles Amplify Systemic Inflammation by Thrombin-Dependent Activation of Complement

Miltenberger blood group antigen type III (Mi.III) enhances the expression of band 3

A cytometric study of the red blood cells in Gaucher disease reveals their abnormal shape that may be involved in increased erythrophagocytosis

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