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Erythrocyte programmed cell death
Article first published online: 20 AUG 2008
Copyright © 2008 International Union of Biochemistry and Molecular Biology, Inc.
Volume 60, Issue 10, pages 661–668, October 2008
How to Cite
Föller, M., Huber, S. M. and Lang, F. (2008), Erythrocyte programmed cell death. IUBMB Life, 60: 661–668. doi: 10.1002/iub.106
- Issue published online: 18 SEP 2008
- Article first published online: 20 AUG 2008
- Manuscript Accepted: 25 APR 2008
- Manuscript Received: 20 MAR 2008
- Deutsche Forschungsgemeinschaft. Grant Numbers: La 315/4-3, La 315/6-1, La 315/11-1,2, La 315/13-1, Hu 781/4-3
- red blood cells;
Eryptosis, the suicidal death of erythrocytes, is characterised by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling with phosphatidylserine exposure at the cell surface. Phosphatidylserine-exposing erythrocytes are recognised by macrophages, which engulf and degrade the affected cells. Reported triggers of eryptosis include osmotic shock, oxidative stress, energy depletion, ceramide, prostaglandin E2, platelet activating factor, hemolysin, listeriolysin, paclitaxel, chlorpromazine, cyclosporine, methylglyoxal, amyloid peptides, anandamide, Bay-5884, curcumin, valinomycin, aluminium, mercury, lead and copper. Diseases associated with accelerated eryptosis include sepsis, malaria, sickle-cell anemia, β-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, phosphate depletion, iron deficiency, hemolytic uremic syndrome and Wilsons disease. Eryptosis may be inhibited by erythropoietin, adenosine, catecholamines, nitric oxide (NO) and activation of G-kinase. Most triggers of eryptosis except oxidative stress are effective without activation of caspases. Their signalling involves formation of prostaglandin E2 with subsequent activation of cation channels and Ca2+ entry and/or release of platelet activating factor (PAF) with subsequent activation of sphingomyelinase and formation of ceramide. Ca2+ and ceramide stimulate scrambling of the cell membrane. Ca2+ further activates Ca2+-sensitive K+ channels leading to cellular KCl loss and cell shrinkage and stimulates the protease calpain resulting in degradation of the cytoskeleton. Eryptosis allows defective erythrocytes to escape hemolysis. On the other hand, excessive eryptosis favours the development of anemia. Thus, a delicate balance between proeryptotic and antieryptotic mechanisms is required to maintain an adequate number of circulating erythrocytes and yet avoid noneryptotic death of injured erythrocytes. © 2008 IUBMB IUBMB Life, 60(10): 661–668, 2008