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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interactions of normal erythrocytes and erythrocytes from patients having hemoglobin S hemoglobinopathies with normal human endothelial cells (EC) were investigated under flow conditions. When EC supernatant, containing 2.8-11.0 U/dl of von Willebrand factor (vWF) antigen and vWF multimeric forms larger than those present in normal plasma, was the red blood cell (RBC)-suspending medium instead of serum-free medium (SFM), the adhesion of sickle RBC, but not normal RBC, to endothelial cells was greatly increased (range of enhancement of sickle RBC adhesion, 2- to 27-fold). Adhesion of sickle RBC to endothelial cells was reduced to near serum-free levels when EC supernatant was immunologically depleted of vWF forms. Sickle RBC suspended in SFM containing 200 U/dl of purified vWF multimers of the type found in normal human plasma or 300 micrograms/ml human fibronectin were only slightly more adhesive to endothelial cells than sickle RBC suspended in SFM alone. These data indicate that unusually large vWF multimers produced by endothelial cells are potent mediators of the adhesion of sickle erythrocytes to endothelial cells. Vaso-occlusive crises in sickle cell anemia may be caused, at least in part, by adhesive interactions between the abnormal surfaces of sickle RBC and the endothelium after the release of unusually large vWF multimeric forms from stimulated or damaged endothelial cells.
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PMID:Unusually large von Willebrand factor multimers increase adhesion of sickle erythrocytes to human endothelial cells under controlled flow. 349 53

The abnormal adherence of sickle erythrocytes to endothelial cells (EC) has been hypothesized to play a role in the initiation of vaso-occlusion in sickle cell anemia. We studied erythrocyte/endothelial cell interactions under controlled flow conditions for normal (AA), homozygous sickle cell (SS), sickle cell trait (AS), mechanically injured normal, and "high reticulocyte control" red blood cells (RBC). Human umbilical vein endothelial cells grown to confluence on glass slides formed the base of a parallel plate flow chamber into which RBC suspensions were perfused at a constant flow rate, producing a wall shear stress of 1 dyne/cm2. Adhesion was monitored using video microscopy, and the number of adherent RBC was determined at ten-minute intervals during a wash out period. Results indicate that SS RBC were more adherent than AA RBC. Mechanically injured (sheared) RBC were also more adherent than control normal cells, but less adherent than SS RBC. AS RBC did not differ significantly in their adhesive properties from normal RBC. Less dense (younger) RBC were more adherent to EC than dense (older) cells for normal, SS and "high reticulocyte control" RBC. These findings suggest that the increased adhesion of sickle RBC is at least partially related to the increased numbers of young RBC present. Increased adherence of young cells to the EC lining vessel walls could contribute to microvascular occlusion by lengthening vascular transit times of other sickle cells. Microvascular occlusion is a major clinical problem in sickle cell anemia. This obstruction to blood flow could be due to decreased deformability of the cell and its inability to pass through small vessels. If this were the case it would be reasonable to expect that the most severely deformed sickle cells, the irreversibly sickled RBC (ISC), would play an important role in the initiation of vaso-occlusion. However, the number of circulating ISC is not well correlated with the frequency of painful crises and other microvascular occlusive phenomena. Recent evidence suggests that microvascular occlusion may be associated with increased adhesion of sickle cells to vascular endothelial cells. A strong correlation between erythrocyte adherence and clinical vaso-occlusive severity has been reported by Hebbel et al. Hoover et al. and Hebbel et al. demonstrated increased adhesion in static tests.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Rheological studies of erythrocyte-endothelial cell interactions in sickle cell disease. 361 82

In order to determine whether the phenomenon of sickle erythrocyte adherence to cultured vascular endothelium exists under conditions of blood flow, we exposed monolayers of bovine aortic endothelial cells to flowing sickle cell blood under controlled conditions in a specially designed flow chamber. Individual red cells were imaged by means of epifluorescent videomicroscopy, five percent of the total number of red cells in an aliquot of blood having been labelled by the passive uptake of sodium fluorescein isothiocyanate. At a shear rate of 270 sec-1 at the blood-monolayer interface, red cells from sickle cell blood frequently adhered to the monolayer for periods ranging from 100's of m sec to greater than 30 sec. With adhesion defined as the average number of adherent red cells during the sixth minute of blood flow (corrected upward to account for unlabelled erythrocytes), adhesion with sickle cell blood was of the order of 10(4) erythrocytes/cm2 ECM and exceeded (p less than 0.001) that for normal blood by a factor of 5.6. Further studies utilizing in situ displacement of blood with culture medium followed by brightfield microscopy indicate that the adherent cells were predominantly discocytes having single points of tethering to unknown sites on the monolayer. Adhesion of sickle cell erythrocytes to endothelium, therefore, is a very real phenomenon under physiologic conditions of blood flow; this phenomenon may contribute to the pathophysiology of vaso-occlusive events seen in sickle cell disease.
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PMID:Sickle erythrocytes adhere to endothelial cell monolayers (ECM's) exposed to flowing blood. 361 85

Erythrocyte-endothelial cell interactions were rediscovered using endothelial cells in culture and radiolabelled erythrocytes. Increased adherence of erythrocytes from patients with sickle cell anaemia was found to be related to the occurrence of vaso-occlusive episodes. In diabetes mellitus and sickle cell anaemia, the adhesion was shown to be potentiated by plasmatic factors such as fibrinogen and fibronectin and to induce endothelial cell activation and enhanced prostacyclin production. The molecular basis of the abnormal adherence of diabetic erythrocytes was shown to be linked to Advanced Glycosylated End-products (AGE) present on the cell membrane and to RAGE 35 receptors exposed by the endothelium. Intercellular Adhesion Molecule (ICAM) was identified as an ubiquitous receptor present on endothelium and involved in leucocyte adhesion and it was more recently demonstrated that erythrocytes infested by Plasmodium falciparum bind to ICAM. This adhesion may be important for the dissemination of Plasmodium falciparum and the complications of the disease. In summary, interactions between endothelium and erythrocytes appear to be involved in the pathophysiology of a number of affections and could constitute a new therapeutic target.
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PMID:Adhesion of erythrocytes to endothelium in pathological situations: a review article. 797 Dec 46

Increased adhesion of red cells to vascular endothelium has been implicated in the pathogenesis of falciparum malaria and sickle cell disease. We have carried out a comparative study of the adhesiveness of normal (AA), sickle trait (AS), and homozygous sickle (SS) red cells, with and without parasitization by Plasmodium falciparum, with an in vitro flow system. Adhesion of nonparasitized red cells to cultured human umbilical vein endothelial cells (either glutaraldehyde fixed or untreated) was strongly dependent on the wall shear stress. Many AA and SS cells adhered at low stress (0.02 Pa), but far fewer did so when the stress was increased to a physiologic level (0.1 Pa). Compared with AA cells, SS adhered in greater number (about threefold) and required greater stress (about two-fold) for their subsequent removal. In contrast, the efficiency of adhesion of AA cells parasitized by Plasmodium falciparum was essentially constant up to 0.1 Pa, where it was about 1000 times greater than the efficiency for nonparasitized cells. The stress required to remove parasitized cells was about 6 times that for controls. When parasites were grown in SS cells, fewer cells adhered than when parasites were grown in AA cells. However, the adhesion of malarial-parasitised AS cells was only slightly less than that of parasitized AA cells, so that modulation of adhesion is unlikely to underlie the protective effect of sickle gene in malaria. Adhesion of red cells to endothelium may promote blockage of microvessels, and the interaction of parasitized cells appears strong enough to directly cause ischemic complications in falciparum malaria.
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PMID:Comparative study of the adhesion of sickle cells and malarial-parasitized red cells to cultured endothelium. 847 98

The pathophysiology of vaso-occlusive crisis in sickle cell disease involves interactions among blood cells, plasma proteins, and vessel wall components. The initial goal of this work was to quantify the adhesion of sickle red blood cells (RBCs) to fibronectin immobilized on glass under both static and dynamic shear stress conditions. High-power microscopic inspection of static assay plates showed striking numbers of adherent neutrophils as well as RBCs. Sickle neutrophils and RBCs were significantly more adherent to fibronectin than the corresponding normal cells in static adhesion assays. Adhesion of both sickle neutrophils and sickle RBCs in dynamic adhesion assays was promoted by a period of static incubation preceding initiation of shear stress conditions. Adherent neutrophils remained attached at shear stresses up to 51 dyne/cm2; most adherent RBCs were attached at shear stresses up to 13 dyne/cm2, but detached at a shear stress of 20 dyne/cm2. Sickle neutrophil adhesion was enhanced significantly by autologous plasma. Elevated levels of plasma interleukin-6 (IL-6; but not IL-1 or IL-8) were found in 6 of 9 sickle cell disease samples examined, and elevated levels of tumor necrosis factor were found in 2 of 9 samples. Plasma IL-6 levels correlated positively with both the number of sickle neutrophils adherent to fibronectin and the ability of sickle plasma to enhance adhesion of normal neutrophils to fibronectin. These data suggest possible roles for neutrophil activation and for fibronectin in mediating sickle neutrophil and RBC adhesion.
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PMID:Adhesion of sickle neutrophils and erythrocytes to fibronectin. 855 2

Adhesion of sickle erythrocytes to vascular endothelium plays a central role in sickle cell disease complications. Cytokines and adhesion molecules are critically involved in the regulation of these adhesive processes. To analyze their role, IL-6, GM-CSF, sVCAM-1, sICAM-1, sE-Selectin, and sP-Selectin serum levels were determined in sickle cell patients under basic conditions and during vasoocclusive crisis. In nonsymptomatic patients a high serum level of sVCAM-1 was observed compared to controls. In patients having vasoocclusive crisis sVCAM-1 levels increased even more and seemed to correlate with crisis evolution.
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PMID:Enhanced levels of soluble VCAM-1 in sickle cell patients and their specific increment during vasoocclusive crisis. 880 48

Many types of hemolytic anemia may be associated with liver disease. Liver injury can be caused by the adherence of deformed or hemolyzed erythrocyses to hepatic vascular endothelium. Adhesion of large numbers of hemolyzed red blood cells to hepatic macrophages, or occlusion of hepatic sinusoids by fragmented red cells, can also result in injury of the liver. Thrombosis of the hepatic or portal vein is associated with some types of hemolytic anemia, and can cause severe liner injury. These are some examples of hepatic injury that can be caused by hemolytic anemias. This article discusses some aspects of liver disease that is associated with sickle cell anemia, paroxysmal nocturnal hemoglobinuria, glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis, and HELLP syndrome.
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PMID:Anemia and the liver. Hepatobiliary manifestations of anemia. 1251 98

The risk for thrombosis is increased in patients with hereditary hydrocytosis, an uncommon variant of hereditary stomatocytosis. Erythrocytes from 2 patients with hydrocytosis were studied to gain insight into the mechanism of thrombosis in this disorder. Erythrocytes demonstrated abnormal osmotic scan ektacytometry and decreased erythrocyte filtration rates. There was also a mild increase in adherence of erythrocytes to endothelial monolayers in a micropipette assay. Adhesion of erythrocytes to the subendothelial matrix proteins thrombospondin and laminin, however, was not significantly increased. Percentages of hydrocytosis erythrocytes and reticulocytes with phosphatidylserine exposed on the outer surfaces were increased in both patients compared with healthy controls, indicating altered membrane phospholipid asymmetry. Increased phosphatidylserine exposure accelerating thrombin-forming processes has been proposed as a mechanism for thrombosis in sickle cell disease and beta-thalassemia and may play a similar role in hereditary hydrocytosis.
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PMID:Altered erythrocyte endothelial adherence and membrane phospholipid asymmetry in hereditary hydrocytosis. 1256 Feb 40

Microvascular complications in sickle cell disease occur as a result of obstruction of small vessels by deoxygenated sickle cells. Cerebrovascular complications are also common and result from obstruction of large blood vessels by thrombosis with changes in vessels that have some similarity to those found in arteriosclerotic vascular disease. Endothelial damage and activation from sickle cell-endothelial interactions may contribute to both. We find that endothelial cells have increased expression of VCAM-1, E-selectin, and ICAM-1 when exposed to sickle blood cells. The concentration-dependent, sickle-induced, adhesion molecule expression is significantly greater than that promoted by normal cells. The time course of Cell Adhesion Molecule (CAM) expression is similar to that induced by TNF-alpha and IL1. Studies after white cell enrichment and reduction suggest leukocytes are the primary mediators. CAM expression by endothelial cells appears stimulated by soluble factors. Antibody inhibition studies support TNF-alpha and IL-1, produced by sickle leukocytes, as the primary soluble factors responsible for the observed CAM expression. Both the induction of endothelial CAM expression and subsequent endothelial adherence of sickle erythrocytes may play significant roles in the pathophysiology of sickle-related complications, and reduction in CAM expression may provide a new approach to treatment.
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PMID:Activation of vascular endothelial cell adhesion molecule expression by sickle blood cells. 1267 44


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