Galectin-1, a cell adhesion modulator, induces apoptosis of rat Leydig cells in vitro
Autor: | Berta Denduchis, Vanesa G. Martinez, Selva B. Cigorraga, Eliana Herminia Pellizzari, Carlota Wolfenstein-Todel, M. Mercedes Iglesias, Emilce S. Diaz, Livia Lustig |
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Rok vydání: | 2003 |
Předmět: |
Male
medicine.medical_specialty Galectin 1 Cell Survival Fluorescent Antibody Technique Apoptosis Caspase 3 In Vitro Techniques Biology Biochemistry Flow cytometry Rats Sprague-Dawley Extracellular matrix Internal medicine Testis Cell Adhesion medicine Animals Testosterone Viability assay Cell adhesion Cells Cultured Leydig cell medicine.diagnostic_test Leydig Cells Flow Cytometry In vitro Culture Media Rats Cell biology medicine.anatomical_structure Endocrinology Caspases Colorimetry |
Zdroj: | Glycobiology. 14:127-137 |
ISSN: | 1460-2423 |
DOI: | 10.1093/glycob/cwh025 |
Popis: | 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. |
Databáze: | OpenAIRE |
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