Galectin-1 induces reatlversible 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, Richard D. Cummings

Research output: Contribution to journalArticlepeer-review

72 Scopus citations


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.

Original languageEnglish
Pages (from-to)1408-1418
Number of pages11
JournalMolecular biology of the cell
Issue number5
StatePublished - Mar 1 2009


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