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Erythrocyte Aging: A More than Superficial Resemblance to Apoptosis?Bosman G.J.C.G.M.1 · Willekens F.L.A.2 · Werre J.M.3
1Department of Biochemistry, Radboud University Nijmegen Medical Center, Nijmegen Center for Molecular Life Sciences, 2Department of Clinical Chemistry, Rijnstate Hospital, Arnhem, 3Department of Blood Transfusion and Transplantation Immunology, Radboud University Nijmegen Medical Center Corresponding Author
Dr. G. Bosman, Ph.D.
Dept. Biochemistry (160), Radboud Uni Med Center Nijmegen
P.O. Box 9101, NL-6500 HB Nijmegen (The Netherlands)
Tel. +31-24-3615390/14259, Fax: +31-24-3616413
In physiological circumstances, erythrocyte aging leads to binding of autologous IgG followed by recognition and removal through phagocytosis, mainly by Kupffer cells in the liver. This process is triggered by the appearance of a senescent erythrocyte-specific antigen. The functional and structural characteristics of senescent erythrocytes strongly suggest that this antigen originates on band 3, probably by calcium-induced proteolysis. Generation of vesicles enriched in denatured hemoglobin is an integral part of the erythrocyte aging process. These versicles are also removed by Kupffer cells, with a major role for exposure of phosphatidylserine. Moreover, senescent erythrocyte-specific antigens are present on vesicles. Thus, vesicles and senescent erythrocytes may be recognized and removed through the same signals. These and other, recent data support the theory that erythrocyte aging is a form of apoptosis that is concentrated in the cell membrane, and provide the context for future studies on initation and regulation of the erythrocyte aging process. Insight into the normal aging mechanism is essential for understanding the fate of erythrocytes in pathological circumstances and the survival of donor erythrocytes after transfusion.
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