Galectin-1 Induces Reversible Phosphatidylserine Exposure at the Plasma Membrane

• Type of Material: Article
• Authors: Sean R. Stowell, Emory University; Sougata Karmakar, Oklahoma Medical Research Foundation; Connie Arthur, Emory University; Tongzhong Ju, Emory University; Lilian C. Rodrigues, University of Sao Paulo; Thalita B. Riul, University of Sao Paulo; Marcelo Dias-Baruffi, University of Sao Paulo; Jonathan Miner, Oklahoma Medical Research Foundation; Rodger P. McEver, Oklahoma Medical Research Foundation; Richard Cummings, Emory University
• Language: English
• Date: 2009-03-01
• Publisher: American Society for Cell Biology
• Publication Version: Final Published Version
• Copyright Statement: © 2009 by The American Society for Cell Biology
• Final Published Version (URL): http://www.molbiolcell.org/content/20/5/1408
• Title of Journal or Parent Work: Molecular Biology of the Cell
• ISSN: 1059-1524
• Volume: 20
• Issue: 5
• Start Page: 1408
• End Page: 1418
• Grant/Funding Information: This work was supported by National Institutes of Health Grant HL085607 to R.P.M. and R.D.C.
• Research Categories: Chemistry, Biochemistry

Abstract

Cells normally undergo physiological turnover through the induction of apoptosis and phagocytic removal, partly through exposure of cell surface phosphatidylserine (PS). In contrast, neutrophils appear to possess apoptosis-independent mechanisms of removal. Here we show that Galectin-1 (Gal-1) induces PS exposure independent of alterations in mitochondrial potential, caspase activation, or cell death. Furthermore, Gal-1–induced PS exposure reverts after Gal-1 removal without altering cell viability. Gal-1–induced PS exposure is uniquely microdomain restricted, yet cells exposing PS do not display evident alterations in membrane morphology nor do they exhibit bleb formation, typically seen in apoptotic cells. Long-term exposure to Gal-1 prolongs PS exposure with no alteration in cell cycle progression or cell growth. These results demonstrate that Gal-1–induced PS exposure and subsequent phagocytic removal of living cells represents a new paradigm in cellular turnover.