Altered membrane phospholipid organization and erythrophagocytosis in E beta-thalassemia.
The underlying cause behind the accelerated destruction of erythrocytes in the bone marrow and in the peripheral circulation, accompanying the beta-thalassemic syndromes is still not clearly understood. The present investigation demonstrates that increased phagocytosis of erythrocytes in E beta-thalassemia is inhibited by the presence of phosphatidylserine (PS) vesicles, suggesting a PS-'PS-receptor' type of interaction in premature recognition of these erythrocytes by macrophages. Increased exposure of both aminophospholipids phosphatidylethanolamine (PE) and PS was demonstrated by fluorescamine labeling and annexin binding, respectively. The slower rate of translocation of PS across the bilayer suggested that this contributed towards the increased exposure of PS in E beta-thalassemic erythrocytes.
Srinivasan
P T
PT
Department of Chemistry, Bose Institute, Calcutta, India.
Basu
J
J
D017302:Annexins / Q000097:blood; D004910:Erythrocyte Membrane / Q000737:chemistry* / Q000648:ultrastructure; D006446:Hemoglobin E; D006801:Humans; D008051:Lipid Bilayers; D008264:Macrophages / Q000502:physiology; D010587:Phagocytosis; D010714:Phosphatidylethanolamines / Q000097:blood; D010718:Phosphatidylserines / Q000097:blood*; D013499:Surface Properties; D017086:beta-Thalassemia / Q000097:blood*
D017302:Annexins; D008051:Lipid Bilayers; D010714:Phosphatidylethanolamines; D010718:Phosphatidylserines; D006446:Hemoglobin E