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Glycobiology Advance Access originally published online on November 24, 2003
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Glycobiology vol 14 no 2 pp. 127-137, 2004
© Oxford University Press 2004; all rights reserved.

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

Vanesa G. Martinez2, Eliana H. Pellizzari3, Emilce S. Díaz4, Selva B. Cigorraga3, Livia Lustig4, Berta Denduchis4, Carlota Wolfenstein-Todel2 and M. Mercedes Iglesias1,2

2 Instituto de Química y Fisicoquómica Biológicas (UBA-CONICET), Facultad de Farmacia y Bioquómica, Universidad de Buenos Aires, Junón 956, (1113) Buenos Aires, Argentina; 3 Centro de Investigaciones Endocrinológicas (CONICET), Hospital de Niños ìRicardo Gutierrez, Gallo 1330, (1425) Buenos Aires, Argentina; and 4 Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, (1121) Buenos Aires, Argentina

Received on June 12, 2003; revised on July 7, 2003; accepted on October 16, 2003

Galectin-1 (Gal-1), a beta galactoside-binding lectin, is involved in multiple biological functions, such as cell adhesion, apoptosis, and metastasis. On the basis of its ability to interact with extracellular matrix (ECM) glycoproteins, we investigated the 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, under both 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 with 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 us better understand the molecular basis of Leydig cell function and survival control.

1 To whom correspondence should be addressed; e-mail: miglesia{at}qb.ffyb.uba.ar


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