Enhanced adherence of β‐thalassaemic erythrocytes to endothelial cells

Hovav, Tavor; Goldfarb, Ada; Artmann, G.M.; Yedgar, Saul; Barshtein, Gregory

doi:10.1046/j.1365-2141.1999.01489.x

Cited by 81 publications

(58 citation statements)

References 11 publications

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“…45 RBCs from patients with ␤-TM and ␤-TI showed enhanced adhesion to cultured ECs (10-to 25-fold increase compared to normal RBCs). 46 Similar findings were described in SCD 45,47 where the interaction of sickle RBCs with ECs induced a state of oxidative stress leading to enhanced transendothelial migration of blood monocytes. 48 Monocyte activation may also play a significant role in heightening endothelial activation or injury in both thalassemia and SCD.…”

Section: Endothelial Monocyte and Granulocyte Activationsupporting

confidence: 72%

The hypercoagulable state in thalassemia

Eldor

Rachmilewitz

2002

Blood

440

376

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Thalassemia is a congenital hemolytic disorder caused by a partial or complete deficiency of ␣-or ␤-globin chain synthesis. Homozygous carriers of ␤-globin gene defects suffer from severe anemia and other serious complications from early childhood. The disease is treated by chronic blood transfusion. However, this can cause severe iron overload resulting in progressive organ failure. Some forms of ␣ thalassemia are also associated with a similar clinical picture. Despite the difficulties associated with treatment, standards of care for thalassemic patients have improved in recent years, resulting in almost doubling of the average life expectancy. As a consequence, additional previously undescribed, complications are now being recognized. In particular, profound hemostatic changes have been observed in patients with ␤-thalassemia major (␤-TM) and ␤-thalassemia intermedia (␤-TI) and also in patients with ␣ thalassemia (hemoglobin H disease). The presence of a higher than normal incidence of thromboembolic events, mainly in ␤-TI, and the existence of prothrombotic hemostatic anomalies in the majority of the patients, even from a very young age, have led to the recognition of the existence of a chronic hypercoagulable state in thalassemic patients. Despite the appearance of numerous publications on the frequent occurrence of thromboembolic complications in thalassemia, this complication has not been emphasized or comprehensively reviewed. This review summarizes the current literature and discusses possible mechanisms of the lifelong hypercoagulable state that exists in thalassemia. (Blood. 2002;99:36-43)

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Section: Endothelial Monocyte and Granulocyte Activationsupporting

confidence: 72%

The hypercoagulable state in thalassemia

Eldor

Rachmilewitz

2002

Blood

440

376

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“…For example, using the same system applied here, we have found that the adherence of thalassemic or cold-stored RBCs is enhanced by 10-and 8-fold, respectively (21,30). Similarly, RBC deformability is markedly reduced during blood banking procedures, since the percentage of undeformable RBCs was increased to 4% during cold storage and up to 40% by ␥-irradiation (30).…”

Section: Discussionmentioning

confidence: 71%

Additive effect of red blood cell rigidity and adherence to endothelial cells in inducing vascular resistance

Kaul

Koshkaryev²,

Artmann³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Kaul DK, Koshkaryev A, Artmann G, Barshtein G, Yedgar S. Additive effect of red blood cell rigidity and adherence to endothelial cells in inducing vascular resistance. Am J Physiol Heart Circ Physiol 295: H1788 -H1793, 2008. First published August 29, 2008 doi:10.1152/ajpheart.253.2008.-To explore the contribution of red blood cell (RBC) deformability and interaction with endothelial cells (ECs) to circulatory disorders, these RBC properties were modified by treatment with hydrogen peroxide (H2O2), and their effects on vascular resistance were monitored following their infusion into rat mesocecum vasculature. Treatment with 0.5 mM H2O2 increased RBC/EC adherence without significant alteration of RBC deformability. At 5.0 mM H2O2, RBC deformability was considerably reduced, inducing a threefold increase in the number of undeformable cells, whereas RBC/EC adherence was not further affected by the increased H2O2 concentration. This enabled the selective manipulation of RBC adherence and deformability and the testing of their differential effect on vascular resistance. Perfusion of RBCs with enhanced adherence and unchanged deformability (treatment with 0.5 mM H2O2) increased vascular resistance by about 35% compared with untreated control RBCs. Perfusion of 5.0 mM H 2O2-treated RBCs, with reduced deformability (without additional increase of adherence), further increased vascular resistance by about 60% compared with untreated control RBCs. These results demonstrate the specific effects of elevated adherence and reduced deformability of oxidized RBCs on vascular resistance. These effects can be additive, depending on the oxidation conditions. The oxidation-induced changes applied in this study are moderate compared with those observed in RBCs in pathological states. Yet, they caused a considerable increase in vascular resistance, thus demonstrating the potency of RBC/EC adherence and RBC deformability in determining resistance to blood flow in vivo. erythrocyte rheology; aggregability; adhesion; circulatory disorders RED BLOOD CELLS (RBCs) have special flow-affecting properties that are major determinants of blood flow: deformability, RBC-RBC aggregability, and RBC/endothelial cell (EC) adherence.

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“…These findings are indicative of the membrane changes, leading to enhanced ability of thalassemic RBCs to adhere to ECs, especially in a-and b-thal carriers. Enhanced adhesion of b-thalassemia major and b-thalassemia intermedia RBCs to ECs has also been recently reported (33).…”

Section: Discussionmentioning

confidence: 96%

Cytoadherence between endothelial cells and P. falciparum infected and noninfected normal and thalassemic red blood cells

Butthep¹,

Wanram²,

Pattanapanyasat³

et al. 2006

Cytometry Part B Clinical

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Background: Cytoadhesion of P. falciparum infected red blood cells (RBCs) to endothelial cells (ECs)is an important phenomenon that causes cerebral malaria in man. Reduced adhesion especially in thalassemia and hemoglobinopathies may be related to a protective mechanism against malaria in such people.Methods: The cytoadherence assay was performed using both conventional and floating conditions between ECs (ECV 304) and P. falciparum infected and noninfected RBCs from both normal and thalassemia subjects. In floating condition, RBC was fluorescently labeled with anti-glycophorin A antibody, whereas EC was identified by surface expression of PECAM-1, CD-36, ICAM-1, and E-selectin. The condition of floating EC was similar to the condition for subcultivation as they can adhere or bind to any surface. The phosphatidylserine (PS) exposure was also determined by using flow cytometer.Results: The adhesion of noninfected heterozygous thalassemic RBCs (all genotypes) to ECs was significantly increased as compared with normal RBCs (P < 0.02). Interestingly, after P. falciparum infection, the number of normal RBCs bound to ECs was significantly increased as compared with noninfected RBCs (P < 0.01), whereas heterozygous thalassemic RBCs infected by P. falciparum showed no significant difference compared with noninfected RBCs. In addition, we found a similar level of PS exposure in normal and thalassemic infected RBCs, which was related to the cytoadherence phenomenon.Conclusion: The reduced adhesion between heterozygous thalassemic RBCs infected by P. falciparum to ECs provides an explanation for their protective mechanism against malaria, as increased adhesion is a high risk for cerebral malaria and nonbinding infected RBCs can be removed by the reticuloendothelial system and other mechanism(s) in vivo. q

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Enhanced adherence of β‐thalassaemic erythrocytes to endothelial cells

Cited by 81 publications

References 11 publications

The hypercoagulable state in thalassemia

The hypercoagulable state in thalassemia

Additive effect of red blood cell rigidity and adherence to endothelial cells in inducing vascular resistance

Cytoadherence between endothelial cells and P. falciparum infected and noninfected normal and thalassemic red blood cells

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