Uncoupling of the spectrin-based skeleton from the lipid bilayer in sickled red cells.

The distribution of spectrin and band 3 in deoxygenated reversibly sickled cells was visualized by immunofluorescence and immunoelectron microscopy. Antibodies against band 3, the major lipid-associated transmembrane protein, labeled the entire cell body, including the entire length of the long protruding spicule, whereas antibodies against spectrin labeled only the cell body and the base region of the spicules. The results suggest that the formation of long spicules during sickling is associated with a continuous polymerization of hemoglobin S polymers, presumably through gaps in the spectrin-actin meshwork, and a subsequent uncoupling of the lipid bilayer from the submembrane skeleton.

[1]  N. Mohandas,et al.  Association between morphologic distortion of sickle cells and deoxygenation-induced cation permeability increase. , 1986, Blood.

[2]  C. Joiner,et al.  Deoxygenation-induced cation fluxes in sickle cells: relationship between net potassium efflux and net sodium influx. , 1988, Blood cells.

[3]  B. Roelofsen,et al.  Uncoupling of the membrane skeleton from the lipid bilayer. The cause of accelerated phospholipid flip-flop leading to an enhanced procoagulant activity of sickled cells. , 1985, The Journal of clinical investigation.

[4]  B. Lubin,et al.  Red cell vesiculation--a common membrane physiologic event. , 1986, The Journal of laboratory and clinical medicine.

[5]  David Allan,et al.  Release of spectrin-free spicules on reoxygenation of sickled erythrocytes , 1982, Nature.

[6]  H. Goodall Erythrocyte Membranes 2 , 1982 .

[7]  D. Tosteson,et al.  Regulation of erythrocyte cation and water content in sickle cell anemia. , 1986, Science.

[8]  B. Roelofsen,et al.  Studies on sickled erythrocytes provide evidence that the asymmetric distribution of phosphatidylserine in the red cell membrane is maintained by both ATP-dependent translocation and interaction with membrane skeletal proteins. , 1988, Biochimica et biophysica acta.

[9]  M. Canessa,et al.  Deoxygenation inhibits the volume-stimulated, Cl(-)-dependent K+ efflux in SS and young AA cells: a cytosolic Mg2+ modulation. , 1987, Blood.

[10]  P. Thomas,et al.  Ca2+-induced biochemical changes in human erythrocytes and their relation to microvesiculation. , 1981, The Biochemical journal.

[11]  J. Palek,et al.  Release of spectrin-free vesicles from human erythrocytes during ATP depletion: 1. characterization of spectrin-free vesicles , 1977, The Journal of cell biology.

[12]  H. Ris The cytoplasmic filament system in critical point-dried whole mounts and plastic-embedded sections , 1985, The Journal of cell biology.

[13]  W. Coakley,et al.  Vesicle production of heated and stressed erythrocytes. , 1978, Biochimica et biophysica acta.

[14]  Shih-Chun Liu,et al.  Separation of the lipid bilayer from the membrane skeleton during discocyte-echinocyte transformation of human erythrocyte ghosts. , 1989, European journal of cell biology.

[15]  B. Roelofsen,et al.  Effect of dimyristoyl phosphatidylcholine on intact erythrocytes. Release of spectrin-free vesicles without ATP depletion. , 1981, Biochimica et biophysica acta.