Adhesion of normal and sickle erythrocytes to endothelial monolayer cultures

Hoover, Richard L.; Rubin, Robert W.; Wise, Gary E.; Warren, Robert J.

doi:10.1182/blood.v54.4.872.872

Cited by 194 publications

(41 citation statements)

References 12 publications

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“…Red blood cells from patients with sickle cell disease (SS RBC) have abnormally strong adhesive interactions with vessel endothelium and components of the subendothelial matrix. The presence of various cytokines in sickle cell patients, 25‐31 as well as contact of normal RBCs with endothelial cells, causes retraction and/or detachment of endothelial cells 32 and thus may lead to exposure of subendothelial matrix components to circulating cells 33‐36 . SS RBCs adhere abnormally well to several components of the subendothelial matrix, but the strongest interaction is with the heterotrimeric protein laminin 37 .…”

Section: Functional Roles Of B‐cam/lumentioning

confidence: 99%

“…Many studies have shown that SS RBCs adhere more avidly than normal RBCs to cultured endothelial cells, 33,35 , 53 and the increased level of circulating endothelial cells in sickle cell patients also suggests a possible SS RBC interaction with endothelial cells in vivo 36 . Endothelial integrin proteins may be important in the interaction of SS RBCs with endothelial cells, although the precise integrins and the characteristics of these interactions are still under investigation 54 .…”

Section: Functional Roles Of B‐cam/lumentioning

confidence: 99%

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The Lutheran glycoprotein: a multifunctional adhesion receptor

Eyler

Telen

2006

Transfusion

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The Lutheran blood group system, which comprises one of the largest families of human red blood cell (RBC) antigens, resides on two immunoglobulin superfamily (IgSF) proteins: Lutheran and basal cell adhesion molecule (B-CAM). These two glycoproteins arise via alternative splicing of mRNA from a single gene and differ in structure only in the lengths of their cytoplasmic tails. Both are expressed on RBCs as well as a variety of other cell types, and they are overexpressed on sickle RBCs (SS RBC). B-CAM/Lu is the critical receptor for SS RBC adhesion to the extracellular matrix protein laminin, an interaction thought to contribute to the pathogenesis of sickle cell-related vasoocclusive events. Recent work has also shown that B-CAM/Lu on RBCs can undergo activation as a result of adrenergic signaling pathways. The high affinity of B-CAM/Lu for laminin is also thought to contribute to various developmental processes, including organogenesis, vascular development, erythropoiesis, and smooth muscle development and organization. Interestingly, the B-CAM spliceoform seems to be overexpressed by a variety of different malignant tumors and may be involved, along with other adhesion receptor proteins, in malignant transformation and tumor metastasis. Studies of B-CAM/Lu have thus expanded from defining antigen-specific polymorphisms to investigations of processes involved in sickle cell disease, human development, and cancer biology.

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Section: Functional Roles Of B‐cam/lumentioning

confidence: 99%

Section: Functional Roles Of B‐cam/lumentioning

confidence: 99%

The Lutheran glycoprotein: a multifunctional adhesion receptor

Eyler

Telen

2006

Transfusion

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“…The polymerization of deoxygenated HbS results in the formation of rigid and fragile sickle red blood cells (RBCs) responsible for painful vascular occlusion and chronic anaemia, respectively. In addition, sickle RBCs have increased adhesiveness to white blood cells (Belcher et al , ; Frenette, ), platelets (Antonucci et al , ; Wun et al , ) and endothelial cells (Hoover et al , ; Hebbel et al , ), which may participate to the initiation of vaso‐occlusive like events.…”

mentioning

confidence: 99%

Exacerbation of oxidative stress during sickle vaso‐occlusive crisis is associated with decreased anti‐band 3 autoantibodies rate and increased red blood cell‐derived microparticle level: a prospective study

et al. 2016

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Painful vaso-occlusive crisis, a hallmark of sickle cell anaemia, results from complex, incompletely understood mechanisms. Red blood cell (RBC) damage caused by continuous endogenous and exogenous oxidative stress may precipitate the occurrence of vaso-occlusive crises. In order to gain insight into the relevance of oxidative stress in vaso-occlusive crisis occurrence, we prospectively compared the expression levels of various oxidative markers in 32 adults with sickle cell anaemia during vaso-occlusive crisis and steady-state conditions. Compared to steady-state condition, plasma levels of free haem, advanced oxidation protein products and myeloperoxidase, RBC caspase-3 activity, as well as the concentrations of total, neutrophil- and RBC-derived microparticles were increased during vaso-occlusive crises, whereas the reduced glutathione content was decreased in RBCs. In addition, natural anti-band 3 autoantibodies levels decreased during crisis and were negatively correlated with the rise in plasma advanced oxidation protein products and RBC caspase-3 activity. These data showed an exacerbation of the oxidative stress during vaso-occlusive crises in sickle cell anaemia patients and strongly suggest that the higher concentration of harmful circulating RBC-derived microparticles and the reduced anti-band 3 autoantibodies levels may be both related to the recruitment of oxidized band 3 into membrane aggregates.

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“…The reason SCD RBCs cause such damage in the microvasculature through vaso-occlusion and hemolytic anemia is the propensity of sickle (HbS) hemoglobin to polymerize under low oxygen tension [107]. This process changes the shape and rigidity of the RBC membrane as well as its adhesiveness [108].…”

Section: Erythrocyte-endothelium Interfacementioning

confidence: 99%

Vascularized Microfluidics and the Blood–Endothelium Interface

2019

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The microvasculature is the primary conduit through which the human body transmits oxygen, nutrients, and other biological information to its peripheral tissues. It does this through bidirectional communication between the blood, consisting of plasma and non-adherent cells, and the microvascular endothelium. Current understanding of this blood-endothelium interface has been predominantly derived from a combination of reductionist two-dimensional in vitro models and biologically complex in vivo animal models, both of which recapitulate the human microvasculature to varying but limited degrees. In an effort to address these limitations, vascularized microfluidics have become a platform of increasing importance as a consequence of their ability to isolate biologically complex phenomena while also recapitulating biochemical and biophysical behaviors known to be important to the function of the blood-endothelium interface. In this review, we discuss the basic principles of vascularized microfluidic fabrication, the contribution this platform has made to our understanding of the blood-endothelium interface in both homeostasis and disease, the limitations and challenges of these vascularized microfluidics for studying this interface, and how these inform future directions.

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Adhesion of normal and sickle erythrocytes to endothelial monolayer cultures

Cited by 194 publications

References 12 publications

The Lutheran glycoprotein: a multifunctional adhesion receptor

The Lutheran glycoprotein: a multifunctional adhesion receptor

Exacerbation of oxidative stress during sickle vaso‐occlusive crisis is associated with decreased anti‐band 3 autoantibodies rate and increased red blood cell‐derived microparticle level: a prospective study

Vascularized Microfluidics and the Blood–Endothelium Interface

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