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Glycobiology Advance Access published online on June 26, 2009
Glycobiology, doi:10.1093/glycob/cwp077
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Galectin-1 stimulates monocyte chemotaxis via the p44/42 MAP kinase pathway and a Pertussis toxin sensitive pathway

Reshad K. J. Malik, Rohit R. Ghurye, Diana J. Lawrence-Watt and Helen J. S. Stewart

Brighton and Sussex Medical School, University of Sussex, Falmer, Brighton BN1 9PS, Great Britain.

Corresponding author. Tel 0044-1273-877886 Fax 0044-1273-877884, E-mail address H.J.S.Stewart{at}sussex.ac.uk

Received on September 19, 2008; accepted on May 28, 2009

Galectin-1, the prototype of a family of β galactoside-binding proteins, has been implicated in a wide variety of biological processes. Data presented herein show that galectin-1stimulates monocyte migration in a dose dependent manner but is not chemotactic for macrophages. Galectin-1 induced monocyte chemotaxis is blocked by lactose and inhibited by anti galectin-1 antibody but not by non specific antibodies. Furthermore galectin-1 mediated monocyte migration was significantly inhibited by MEK inhibitors in a rapid, time dependent manner suggesting that MAP kinase pathways are involved in galectin-1. Migration was also almost completely blocked by pertussis toxin implying G protein involvement in the galectin-1 induced chemotaxis.

These results demonstrate a role for galectin-1 in monocyte chemotaxis which differs from galectin-3 in that macrophages are non responsive. Furthermore our observations suggest that galectin-1 may be involved in chemoattraction at sites of inflammation in vivo and may contribute to disease processes such as atherosclerosis

Key words: Chemotaxis / Galectin-1 / Monocytes / Signal transduction


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