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Vol. 20, Issue 5, 1408-1418, March 1, 2009

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Galectin-1 Induces Reversible Phosphatidylserine Exposure at the Plasma Membrane

Sean R. Stowell^*, Sougata Karmakar, Connie M. Arthur^*, Tongzhong Ju^*, Lilian C. Rodrigues, Thalita B. Riul, Marcelo Dias-Baruffi, Jonathan Miner, Rodger P. McEver, and Richard D. Cummings^*

*Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322; The Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and Departmento de Análises Clínicas, Toxicológicas e Bromatológicas da Faculdade de Ciências Farmacêuticas de Ribeirão Preto, University of Sao Paulo, Ribeirão Preto-SP, Brazil

Submitted July 31, 2008; Revised November 13, 2008; Accepted December 22, 2008
Monitoring Editor: Donald D. Newmeyer

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.

Address correspondence to: Richard D. Cummings (rdcummi{at}emory.edu)

Abbreviations used: An-V, annexin V; Camp, camptothecin; CFSE, carboxyfluorescein diacetate, succinimidyl ester; DTT, dithiothreitol; Gal-1, galectin-1; Gal-3, galectin-3; Gal-9, galectin-9; PARP, poly(ADP-ribose) polymerase; PI, propidium iodide; PS, phosphatidylserine; SEM, scanning electron microscopy; TNF, tumor necrosis factor.