Premium
Non‐apoptotic phosphatidylserine externalization induced by galectin‐1 in leukocytes is distinct from that accompanying apoptotic cell death.
Author(s) -
Stowell Sean Robinson,
Karmakar Sougata,
McEver Rodger,
Cummings Richard
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a914-b
Subject(s) - phosphatidylserine , apoptosis , microbiology and biotechnology , galectin , intracellular , programmed cell death , phagocytosis , cytosol , chemistry , homeostasis , annexin , biology , biochemistry , enzyme , membrane , phospholipid
The factors responsible for regulating neutrophil homeostasis are poorly understood. Several studies have suggested that non‐apoptotic mechanisms may play a role. However, the elements responsible for the regulation of non‐apoptotic turnover are unknown. We recently showed that galectin‐1, a soluble mammalian lectin highly expressed in endothelial cells, induces the externalization of phosphatidylserine (PS), in activated, but not resting, neutrophils. Importantly, galectin‐1 induced PS exposure occurs in the absence of cell death, although it primes neutrophils for phagocytic removal. Galectin‐1 binds extended sialylated poly‐N‐acetyllactosamine sequences on leukocytes [Leppanen, Stowell, Blixt and Cummings (2005) J. Biol. Chem. 280:5549–62] and induced PS exposure through the activation of Src kinases, phospholipase C gamma and mobilized intracellular calcium [Karmaker, Cummings and McEver (2005) J. Biol. Chem. 280:28623–31]. Because galectin‐1‐induced PS exposure occurs in the absence of apoptosis, we have sought to further define this unique pathway. Here we report the general features of galectin‐1 induced PS exposure and compare this unique mechanism to the externalization of PS accompanying apoptosis. An understanding of this pathway provides new information about the potential biological roles of galectins in regulating leukocyte turnover and homeostasis.