[Critical role of phosphatidylserine in hemolysis due to red blood cell enzyme/membrane defects].
The life span of human red blood cells (RBCs) is approximately for 120 days, and finally destroyed in reticuloendothelial systems. In pathological conditions, RBCs fall into premature death, i.e. hemolysis. Recent studies have unveiled that abnormal RBCs affected by either membrane disorders or enzyme deficiency as well as senescent RBCs shared the common feature, i.e. exposure of phosphatidylserine (PS) in the outer leaflet of the RBC membrane. Increased intracellular oxidative stress or enhanced calcium permeability impairs maintenance of phospholipid asymmetry, resulting in PS externalization. PS and other eat-me signals may contribute to recognition of abnormal RBC by macrophage. In this review, recent understanding of mechanisms underlying hemolysis are discussed.
Kanno
Hitoshi
H
Department of Transfusion Medicine and Cell Processing, and Institute of Medical Genetics, Tokyo Women's Medical University.
D000743:Anemia, Hemolytic / Q000097:blood / Q000209:etiology*; D000818:Animals; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D004910:Erythrocyte Membrane / Q000378:metabolism; D004912:Erythrocytes / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D006461:Hemolysis; D006801:Humans; D008264:Macrophages / Q000276:immunology; D051379:Mice; D018384:Oxidative Stress; D010587:Phagocytosis; D010718:Phosphatidylserines / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
D010718:Phosphatidylserines; D002118:Calcium