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Prepublished online as a Blood First Edition Paper on August 1, 2002; DOI 10.1182/blood-2002-02-0500. This Article Full Text (PDF) All Versions of this Article: 2002-02-0500v1 101/2/747    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Willekens, F L A Articles by Werre, J M Search for Related Content PubMed PubMed Citation Articles by Willekens, F L A Articles by Werre, J M Social Bookmarking                   What's this? Submitted February 14, 2002 Accepted July 24, 2002 Hemoglobin loss from erythrocytes in vivo results from spleen facilitated vesiculation F L A Willekens, B Roerdinkholder-Stoelwinder, Y A M Groenen-Dopp, H J Bos, G J C G M Bosman, A G van den Bos, A J Verkleij, and J M Werre* Department of Clinical Chemistry, Rijnstate Hospital, Arnhem, The Netherlands Sanquin Blood Bank Zuid Oost Nederland, Nijmegen, The Netherlands; Department for Bloodtransfusion and Transplantation Immunology, University Medical Center, Nijmegen, The Netherlands Sanquin Blood Bank Zuid Oost Nederland, Nijmegen, The Netherlands Department of Biochemistry, University Medical Center, Nijmegen, The Netherlands Department for Bloodtransfusion and Transplantation Immunology, University Medical Center, Nijmegen, The Netherlands Department of Molecular Cellbiology, University of Utrecht, Utrecht, The Netherlands * Corresponding author; email: www.R.Moerel{at}utdts.azn.nl. Previous studies have shown that approximately 20% of hemoglobin leaves the circulating red blood cell (RBC), mainly during the second half of its life span. As hemoglobin-containing vesicles are known to circulate in plasma, vesicles were isolated from plasma obtained by pheresis. Flow cytometry studies showed that most RBC-derived vesicles contain hemoglobin. All hemoglobin components were present. Their composition resembled that of old RBC. RBC cohort studies, using isotope-labelled glycine, have been described to show a continuous presence of the label in hemoglobin degradation products, with an increase in the second half of the RBC life span, and a concomitant decrease of the label concentration in the RBC. It was therefore concluded that the hemoglobin loss from circulating RBC of all ages can be explained by shedding of hemoglobin-containing vesicles. This loss occurs predominantly from older RBC. Apparently the spleen facilitates this process as in asplenia vesicle retention in RBC of all ages has been described, together with an increase in the percentage of total HbA1. In the present study it is shown that in old RBC of asplenic individuals there is an absence of the decrease of MCH such as found in old RBC of control individuals, and that this absence is related to an increase in the absolute amount of HbA1c and HbA1e2. This is in accordance with the assumption that vesicles within old RBC contain denatured, membrane-bound hemoglobin, which cells for that reason are more prone to be "pitted" by the spleen. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. M. Cohen, R. S. Franco, P. K. Khera, E. P. Smith, C. J. Lindsell, P. J. Ciraolo, M. B. Palascak, and C. H. Joiner Red cell life span heterogeneity in hematologically normal people is sufficient to alter HbA1c Blood, November 15, 2008; 112(10): 4284 - 4291. [Abstract] [Full Text] [PDF] S. Sadallah, C. Eken, and J. A. Schifferli Erythrocyte-derived ectosomes have immunosuppressive properties J. Leukoc. Biol., November 1, 2008; 84(5): 1316 - 1325. [Abstract] [Full Text] [PDF] J. Galletti, C. Canones, P. Morande, M. Borge, P. Oppezzo, J. Geffner, R. Bezares, R. Gamberale, and M. Giordano Chronic Lymphocytic Leukemia Cells Bind and Present the Erythrocyte Protein Band 3: Possible Role as Initiators of Autoimmune Hemolytic Anemia J. Immunol., September 1, 2008; 181(5): 3674 - 3683. [Abstract] [Full Text] [PDF] F. L. A. Willekens, J. M. Werre, J. K. Kruijt, B. Roerdinkholder-Stoelwinder, Y. A. M. Groenen-Dopp, A. G. van den Bos, G. J. C. G. M. Bosman, and T. J. C. van Berkel Liver Kupffer cells rapidly remove red blood cell-derived vesicles from the circulation by scavenger receptors Blood, March 1, 2005; 105(5): 2141 - 2145. [Abstract] [Full Text] [PDF] E. M. Sloand, L. Mainwaring, K. Keyvanfar, J. Chen, J. Maciejewski, H. G. Klein, and N. S. Young Transfer of glycosylphosphatidylinositol-anchored proteins to deficient cells after erythrocyte transfusion in paroxysmal nocturnal hemoglobinuria Blood, December 1, 2004; 104(12): 3782 - 3788. [Abstract] [Full Text] [PDF]

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