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Glycobiology Advance Access published online on June 12, 2006
Glycobiology, doi:10.1093/glycob/cwl013
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
Received January 27, 2006
Revised May 29, 2006
Accepted June 7, 2006

Article

Galectin-1: Biphasic growth regulation of Leydig tumor cells

Verónica A. Biron 1, M. Mercedes Iglesias 1, María F. Troncoso 1, Marcos Besio-Moreno 2, Zoraida J. Patrignani 2, Omar P. Pignataro 3, and Carlota Wolfenstein-Todel 1 *

1 Instituto de Química y Fisicoquímica Biológicas (UBA-CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956, (1113) Buenos Aires, Argentina
2 Laboratorio de Endocrinología Molecular y Transducción de Señales, Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, (1428) Buenos Aires, Argentina
3 Laboratorio de Endocrinología Molecular y Transducción de Señales, Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, (1428) Buenos Aires, Argentina; Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Pabellón II, Ciudad Universitaria, (1428) Buenos Aires, Argentina

* To whom correspondence should be addressed.
Carlota Wolfenstein-Todel, E-mail: cwtodel{at}mail.retina.ar


  Abstract

Galectin-1 (Gal-1) is a widely expressed {beta}-galactoside binding protein that exerts pleiotropic biological functions. To gain insight into the potential role of Gal-1 as a novel modulator of Leydig cells, we investigated its effect on the growth and death of MA-10 tumor Leydig cells. In this study, we identified cytoplasmic Gal-1 expression in these tumor cells by cytofluorometry. DNA fragmentation, caspase-3, -8 and -9 activation, loss of mitochondrial membrane potential, cytochrome c release and FasL expression suggested that relatively high concentrations of exogenously added recombinant Gal-1 induced apoptosis by the mitochondrial and death receptor pathways. These pathways were independently activated, as the presence of the inhibitor of caspase-8 or -9 only partially prevented Gal-1-effect. On the other hand, low concentrations of Gal-1 significantly promoted cell proliferation, without inducing cell death. Importantly, the presence of the disaccharide lactose prevented Gal-1 effects, suggesting the involvement of the carbohydrate recognition domain. The present study provides strong evidence that Gal-1 is a novel biphasic regulator of Leydig tumor cell number, suggesting a novel role for Gal-1 in the reproductive physiopathology.

Keywords: apoptosis/galectin-1/Leydig cells/proliferation.
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