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Prepublished online as a Blood First Edition Paper on February 27, 2003; DOI 10.1182/blood-2002-11-3416. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-11-3416v1 102/1/365    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Yasin, Z. Articles by Franco, R. S. Search for Related Content PubMed PubMed Citation Articles by Yasin, Z. Articles by Franco, R. S. Related Collections Hemostasis, Thrombosis, and Vascular Biology Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 July 2003, Vol. 102, No. 1, pp. 365-370 RED CELLS Phosphatidylserine externalization in sickle red blood cells: associations with cell age, density, and hemoglobin F Zahida Yasin, Scott Witting, Mary B. Palascak, Clinton H. Joiner, Donald L. Rucknagel, and Robert S. Franco From the Division of Hematology/Oncology, Department of Internal Medicine; the Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine; the Cincinnati Comprehensive Sickle Cell Center; and the Children's Hospital Research Foundation, Cincinnati, OH. Phosphatidylserine (PS) is normally confined to the cytoplasmic leaflet of the red blood cell (RBC) membrane, but some sickle RBCs expose PS in the outer leaflet (PS+ cells). This study examined the relationships among PS externalization, fetal hemoglobin content, hydration state, and cell age. Sickle RBCs exhibit a wide range of PS externalization. Those with low-level exposure (type 1 PS+) include many young transferrin-receptor-positive (TfR+) cells. This is not specific for sickle cell disease because many nonsickle TfR+ cells are also PS+. RBCs with higher PS exposure (type 2 PS+) appear to be more specific for sickle cell disease. Their formation is most likely sickling dependent because type 2 PS+ dense sickle cells have a lower percentage of fetal hemoglobin (HbF) than PS- cells in the same density fraction (1.7 vs 2.9; n = 8; P < .01). In vivo experiments using biotin-labeled sickle cells showed a sharp decrease in the percentage of circulating, labeled PS+ cells in the first 24 hours after reinfusion. This decrease was confined to type 1 PS+ cells and was thus consistent with the reversal of PS exposure in very young cells. As the labeled cells aged in the circulation, the percentages of type 1 and type 2 PS+ cells increased. These studies indicate that PS externalization in sickle cells may be low level, as observed in many immature cells, or high level, which is associated with dehydration and appears to be more specific for sickle RBCs. (Blood. 2003;102: 365-370) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Guchhait, S. K Dasgupta, A. Le, S. Yellapragada, J. A. Lopez, and P. Thiagarajan Lactadherin mediates sickle cell adhesion to vascular endothelial cells in flowing blood Haematologica, September 1, 2007; 92(9): 1266 - 1267. [Abstract] [Full Text] [PDF] M. Minetti, L. Agati, and W. Malorni The microenvironment can shift erythrocytes from a friendly to a harmful behavior: Pathogenetic implications for vascular diseases Cardiovasc Res, July 1, 2007; 75(1): 21 - 28. [Abstract] [Full Text] [PDF] J. Haynes Jr., B. Obiako, J. A. King, R. B. Hester, and S. Ofori-Acquah Activated neutrophil-mediated sickle red blood cell adhesion to lung vascular endothelium: role of phosphatidylserine-exposed sickle red blood cells Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1679 - H1685. [Abstract] [Full Text] [PDF]

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