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Abnormalities in Membrane Phospholipid Organization in Sickled Erythrocytes

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TLDR
The results indicate that the process of sickling induces an abnormality in the organization of membrane lipids in RSC which become permanent in ISC, and the distribution of glycerophospholipids within the membrane of sickled cells is different from that in nonsickled cells.
Abstract
In contrast to the wealth of information concerning membrane phospholipid asymmetry in normal human erythrocytes, very little is known about membrane phospholipid organization in pathologic erythrocytes. Since the spectrin-actin lattice, which has been suggested to play an important role in stabilizing membrane phospholipid asymmetry, is abnormal in sickled erythrocytes, we determined the effects of sickling on membrane phospholipid organization. We used two enzymatic probes: been venom phospholipase A2 and Staphylococcus aureus sphingomyelinase C, which do not penetrate the membrane and react only with phospholipids located in the outer leaflet of the bilayer. Our results suggest that the distribution of glycerophospholipids within the membrane of sickled cells is different from that in nonsickled cells. Compared with the normal erythrocyte, the outer membrane leaflet of the deoxygenated, reversibly sickled cells (RSC) and irreversibly sickled cells (ISC) was enriched in phosphatidyl ethanolamine in addition to containing phosphatidyl serine. These changes were compensated for by a decrease in phosphatidyl choline in that layer. The distribution of sphingomyelin over the two halves of the bilayer was unaffected by sickling. In contrast to ICS, where the organization of phospholipids was abnormal under both oxy and deoxy conditions, reoxygenation of RSC almost completely restored the organization of membrane phospholipids to normal. These results indicate that the process of sickling induces an abnormality in the organization of membrane phospholipids to normal. These results indicate that the process of sickling induces an abnormality in the organization of membrane lipids in RSC which become permanent in ISC.

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Elevated expression of phosphatidylserine in the outer membrane leaflet of human tumor cells and recognition by activated human blood monocytes.

TL;DR: A role for PS is suggested in monocyte recognition of tumor cells through enhanced PS expression on the tumor cells was responsible for their recognition by activated monocytes.
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Regulation of transbilayer plasma membrane phospholipid asymmetry.

TL;DR: It is shown that the flippase is highly selective for phosphatidylserine and functions to keep this lipid sequestered from the cell surface, and the ABC class of transmembrane transporters, at least two members of this class display selectivity for their substrate lipid.
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Increased erythrocyte phosphatidylserine exposure in sickle cell disease: flow-cytometric measurement and clinical associations

TL;DR: Increased exposure of PS on a subpopulation of erythrocytes in vivo is a virtually universal feature of sickle cell disease, and its measurement may be useful to evaluate clinical status and response to therapeutic measures such as blood transfusion.
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Spontaneous oxygen radical generation by sickle erythrocytes.

TL;DR: Data suggest that an excessive accumulation of oxidant damage in sickle erythrocyte membranes might contribute to the accelerated membrane senescence of these cells, and indicate that accumulation of oxidation could be a determinant of normal ery Throcyte membraneSenescence.
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Oxygen radicals stimulate intracellular proteolysis and lipid peroxidation by independent mechanisms in erythrocytes.

TL;DR: Increased proteolysis seems to occur independently of membrane damage and to be a more sensitive indicator of cell exposure to oxygen radicals than is lipid peroxidation.
References
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Journal ArticleDOI

Improved procedure for the extraction of lipids from human erythrocytes.

TL;DR: In this article, a procedure for the extraction of human erythrocyte lipids using chloroform-isopropanol 7:11 (v/v) was described.
Journal ArticleDOI

The removal of leukocytes and platelets from whole blood.

TL;DR: This procedure is rapid, reliable, removes over 99.75 per cent of the leukocytes from blood, and does not seem selectively to retain reticulocytes or to release a significant proportion of leukocyte enzymes.
Journal ArticleDOI

Erythrocyte adherence to endothelium in sickle-cell anemia. A possible determinant of disease severity.

TL;DR: Neither clinical severity nor erythrocyte adherence correlates significantly with red-cell indexes, hemoglobin concentration, percentage of irreversibly sickled red cells, level of fetal hemoglobin, or reticulocyte count, but these findings are consistent with the hypothesis that abnormal interactions between ery throats and endothelium may be the initiating factor in the development of microvascular occlusions in sickle-cell anemia.
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These results indicate that the process of sickling induces an abnormality in the organization of membrane phospholipids to normal.