Erythroid phosphatidyl serine exposure is not predictive of thrombotic risk in mice with hemolytic anemia.

Document Type

Article

Publication Date

2000

Keywords

Anemia-Hemolytic, Animal, Animals-Newborn, Annexin-V, Cell-Size, Erythrocyte-Membrane, Erythrocytes, Flow-Cytometry, Fluorescein-5-isothiocyanate, Lipid-Bilayers, Mice, Mice-Inbred-C57BL, Mice-Mutant-Strains, Phosphatidylserines, Spectrin, Thrombosis

First Page

75

Last Page

83

JAX Source

Blood Cells Mol Dis 2000 Feb; 26(1):75-83.

Grant

CA34193/CA/NCI, F32DK09482/DK/NIDDK, R01HL29305/HL/NHLBI

Abstract

Thrombosis is a major complication of human hemolytic anemias such as sickle cell disease, thalassemia, and severe hereditary spherocytosis (HS). Mice with severe HS and severe hereditary elliptocytosis (HE) also suffer from thrombosis, with incidences ranging from 15 and 22% in beta-spectrin- and ankyrin-deficient mice, respectively, to 85 to 100% in alpha-spectrin-deficient and band 3 knockout mice. A contributing factor to thrombosis could be loss of phospholipid asymmetry of the mutant red blood cells (RBCs), with concomitant exposure of the aminophospholipid phosphatidylserine (PS). Increased PS exposure occurs in RBCs from sickle cell and thalassemia patients and in RBCs from band 3-deficient mice. To determine if increased PS exposure correlates with thrombotic risk in HS and HE mice with ankyrin, beta-spectrin, and alpha-spectrin deficiencies, measurements of FITC-labeled annexin V binding to externalized PS on RBCs were performed. PS exposure is elevated in all mice with HS and HE, but the percentage of RBCs with exposed PS does not correlate with thrombotic risk in these mice. Copyright 2000 Academic Press.

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