Galectin-1 induces reversible phosphatidylserine exposure at the plasma membrane.
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.
Stowell
Sean R
SR
Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.
Karmakar
Sougata
S
Arthur
Connie M
CM
Ju
Tongzhong
T
Rodrigues
Lilian C
LC
Riul
Thalita B
TB
Dias-Baruffi
Marcelo
M
Miner
Jonathan
J
McEver
Rodger P
RP
Cummings
Richard D
RD
D017209:Apoptosis; D002462:Cell Membrane / Q000378:metabolism*; D037483:Galectin 1 / Q000378:metabolism / Q000502:physiology*; D018922:HL-60 Cells; D006801:Humans; D021962:Membrane Microdomains / Q000378:metabolism; D010587:Phagocytosis / Q000502:physiology; D010718:Phosphatidylserines / Q000378:metabolism*; D015398:Signal Transduction
D037483:Galectin 1; C445499:LGALS1 protein, human; D010718:Phosphatidylserines