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Author(s) Dias-Baruffi M; Zhu H; Cho MJ; Karmakar S; McEver RP; Cummings RD Title Dimeric galectin-1 induces surface exposure of phosphatidylserine and phagocytic recognition of leukocytes without inducing apoptosis Source JOURNAL OF BIOLOGICAL CHEMISTRY 278 (42): 41282-41293 Date 2003 OCT 17 Type Journal : Article LCR: 5   NCR: 86   LCS: 1   GCS: 20 Comment   Address Univ Oklahoma, Hlth Sci Ctr, Dept Biochem & Mol Biol, Oklahoma City, OK 73104 USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma Ctr Med Glycobiol, Oklahoma City, OK 73104 USA. Oklahoma Med Res Fdn, Cardiovasc Biol Res Program, Oklahoma City, OK 73104 USA. Univ Sao Paulo, Sch Pharmaceut Sci Ribeirao Preto SP, BR-14015900 Sao Paulo, Brazil. Cheju Natl Univ, Sch Med, Dept Biochem, Cheju 690756, South Korea. Reprint Cummings, RD, Univ Oklahoma, Hlth Sci Ctr, Dept Biochem & Mol Biol, 975 NE 10th St,BRC417, Oklahoma City, OK 73104 USA. Abstract We report that human galectin-1 (dGal-1), a small dimeric beta-galactoside-binding protein, induces phosphatidylserine ( PS) exposure, measured by Annexin V staining, on human promyelocytic HL-60 cells, T leukemic MOLT-4 cells, and fMet-Leu-Phe-activated, but not resting, human neutrophils. This effect of dGal-1 on HL-60 and MOLT-4 cells is enhanced by pretreatment of the cells with neuraminidase, but treatment of resting neutrophils with neuraminidase does not enhance their sensitivity to dGal-1. Although the induction of staining with Annexin V is often associated with apoptosis, the dGal-1-treated HL-60 cells, MOLT-4 cells, and activated neutrophils do not undergo apoptosis, and there is no detectable DNA fragmentation. HL-60 and MOLT-4 cells treated with dGal-1 continue to grow normally. By contrast, camptothecin-treated HL-60 cells, etoposide-treated MOLT-4 cells, and anti-Fas-treated neutrophils exhibit extensive DNA fragmentation and/or cell death. Lactose inhibits the dGal-1-induced effects, indicating that dGal-1-induced signaling requires binding to cell surface beta-galactosides. The dimeric form of Gal-1 is required for signaling, because a monomeric mutant form of Gal-1, termed mGal-1, binds to cells but does not cause these effects. Importantly, dGal-1, but not mGal-1, treatment of HL-60 cells and activated human neutrophils significantly promotes their phagocytosis by activated mouse macrophages. These dGal-1-induced effects are distinguishable from apoptosis, but like apoptotic agents, prepare cells for phagocytic removal. Such effects of dGal-1 may contribute to leukocyte homeostasis. 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