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Glycobiology Advance Access published online on November 24, 2003
Glycobiology, doi:10.1093/glycob/cwh025
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Submitted on June 12, 2003
Revised on July 7, 2003
Accepted on October 16, 2003

© 2003 Oxford University Press

ORIGINAL ARTICLES

Galectin-1, a cell adhesion modulator, induces apoptosis of rat Leydig cells in vitro

Vanesa G. Martinez 1, Eliana H. Pellizzari 2, Emilce S. Díaz 3, Selva B. Cigorraga 2, Livia Lustig 3, Berta Denduchis 3, Carlota Wolfenstein-Todel 1, and M. Mercedes Iglesias 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 Centro de Investigaciones Endocrinológicas (CONICET), Hospital de Niños "Ricardo Gutierrez", Gallo 1330, (1425) Buenos Aires, Argentina
3 Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, (1121) Buenos Aires, Argentina

* To whom correspondence should be addressed. E-mail: miglesia{at}qb.ffyb.uba.ar.

Abstract

Galectin-1 (Gal-1), a beta galactoside-binding lectin, is involved in multiple biological functions like cell adhesion, apoptosis and metastasis. On the basis of its ability to interact with extracellular matrix (ECM) glycoproteins, we investigated Gal-1 effect on Leydig cells, which express and are influenced by ECM proteins. In this study, Gal-1 was identified in Leydig cell cultures by immunofluorescence. To gain insight into its biological role, Gal-1 was added to purified rat Leydig cells, both under basal and human chorionic gonadotrophin-stimulated conditions. Substantial morphological changes were observed and cell viability showed an 80% decrease after 24 h culture. As a functional consequence of Gal-1 addition, testosterone production was reduced in a dose-dependent fashion, reaching a minimum of 26% after 24 h compared to basal values. cAMP showed a similar variation after 3 h. Assessment of DNA hypodiploidy and caspase activity determinations indicated that the reduction in viability and in steroidogenesis was caused by apoptosis induced by Gal-1. Besides, addition of Gal-1 caused Leydig cell detachment. Presence of laminin-1 or lactose prevented the effect of Gal-1, suggesting that the carbohydrate recognition domain is involved in inducing apoptosis. These findings demonstrate a novel mechanism, based on Gal-1 and laminin-1 interaction, which could help to better understand the molecular basis of Leydig cell function and survival control.


apoptosis, galectin-1, laminin-1, Leydig cells, testis
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