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Blood, 1 September 2006, Vol. 108, No. 5, pp. 1611-1617. Prepublished online as a Blood First Edition Paper on May 9, 2006; DOI 10.1182/blood-2005-11-012328. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2005-11-012328v1 108/5/1611    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 Elliott, J. I. Articles by Higgins, C. F. Search for Related Content PubMed PubMed Citation Articles by Elliott, J. I. Articles by Higgins, C. F. Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Phosphatidylserine exposure in B lymphocytes: a role for lipid packing James I. Elliott, Alessandro Sardini, Joanne C. Cooper, Denis R. Alexander, Suzel Davanture, Giovanna Chimini, and Christopher F. Higgins From the Medical Research Council (MRC) Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Hospital Campus, London, United Kingdom; the Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham, Cambridge, United Kingdom; and the Centre d'Immunologie de Marseille-Luminy, Parc Scientifique et Technologique de Luminy, Marseille, France. Plasma membrane lipids are usually distributed asymmetrically, with phosphatidylserine (PS) confined to the inner leaflet. PS exposure at the outer leaflet occurs early in apoptosis, but it is also constitutive on some nonapoptotic cell populations where it plays a role in cell signaling. How PS is transported ("flopped") to the cell surface is unknown. Contrary to previous reports that normal murine B lymphocytes lack lipid asymmetry, we show that PS is normally restricted to the inner leaflet of these cells. PS exposure on normal B cells did, however, occur spontaneously ex vivo. Consistent with the hypothesis that loss of PS asymmetry is regulated by CD45, PS is constitutively exposed on viable, CD45-deficient B cells. We show that calcium-stimulated PS exposure in B cells is strain variable, ABCA1 independent, and both preceded by and dependent on a decrease in lipid packing. This decrease in lipid packing is concomitant with cell shrinkage and consequent membrane distortion, both of which are potently inhibited by blockers of volume-regulatory K+ and Cl- ion channels. Thus, changes in plasma membrane organization precede PS translocation. The data suggest a model in which PS redistribution may occur by a translocase-independent mechanism at energetically favorable sites of membrane perturbation where lipid packing is decreased. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. G. Blankenberg In Vivo Detection of Apoptosis J. Nucl. Med., June 1, 2008; 49(Suppl_2): 81S - 95S. [Abstract] [Full Text] [PDF] S. R. J. Taylor, M. Gonzalez-Begne, S. Dewhurst, G. Chimini, C. F. Higgins, J. E. Melvin, and J. I. Elliott Sequential Shrinkage and Swelling Underlie P2X7-Stimulated Lymphocyte Phosphatidylserine Exposure and Death J. Immunol., January 1, 2008; 180(1): 300 - 308. [Abstract] [Full Text] [PDF] D. Smrz, L. Draberova, and P. Draber Non-apoptotic Phosphatidylserine Externalization Induced by Engagement of Glycosylphosphatidylinositol-anchored Proteins J. Biol. Chem., April 6, 2007; 282(14): 10487 - 10497. [Abstract] [Full Text] [PDF]

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