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Original Paper

Regulation of Phosphatidylserine Exposure in Red Blood Cells

Nguyen D.B.1,2 · Wagner-Britz L.1 · Maia S.1 · Steffen P.3 · Wagner C.3 · Kaestner L.4 · Bernhardt I.1

Author affiliations

1Laboratory of Biophysics, Faculty of Natural and Technical Sciences III, Saarland University, Building A2 4, Saarbruecken,2Department of Molecular Biology, Faculty of Biotechnology, Hanoi University of Agriculture, Ngo Xuan Quang, Gia Lam, Hanoi,3Department of Experimental Physics, Saarland University, Building E2 6, Saarbruecken,4Institute for Molecular Cell Biology, School of Medicine, Saarland University, Building 61, Homburg

Corresponding Author

Ingolf Bernhardt

Universität des Saarlandes, Naturwiss.-Techn. Fakultät III

Zentrales Isotopenlabor / AG Biophysik, Gebäude A2.4

P.O.Box 151150, 66041 Saarbrücken (Germany)

Tel. +49 681 3026689, E-Mail i.bernhardt@mx.uni-saarland.de

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Cell Physiol Biochem 2011;28:847–856

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The exposure of phosphatidylserine (PS) on the outer membrane leaflet of red blood cells (RBCs) serves as a signal for eryptosis, a mechanism for the RBC clearance from blood circulation. The process of PS exposure was investigated as function of the intracellular Ca2+ content and the activation of PKCα in human and sheep RBCs. Cells were treated with lysophosphatidic acid (LPA), 4-bromo-A23187, or phorbol-12 myristate-13 acetate (PMA) and analysed by flow cytometry, single cell fluorescence video imaging, or confocal microscopy. For human RBCs, no clear correlation existed between the number of cells with an elevated Ca2+ content and PS exposure. Results are explained by three different mechanisms responsible for the PS exposure in human RBCs: (i) Ca2+-stimulated scramblase activation (and flippase inhibition) by LPA, 4-bromo-A23187, and PMA; (ii) PKC activation by LPA and PMA; and (iii) enhanced lipid flop caused by LPA. In sheep RBCs, only the latter mechanism occurs suggesting absence of scramblase activity.

© 2011 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: October 28, 2011
Published online: December 15, 2011
Issue release date: December 2011

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

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