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Glycobiology Advance Access originally published online on May 26, 2004
Glycobiology 2004 14(10):871-881; doi:10.1093/glycob/cwh101
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Glycobiology vol. 14 no. 10 © Oxford University Press 2004; all rights reserved.

Effects of galectin-1 on regulation of progesterone production in granulosa cells from pig ovaries in vitro

Hermann Walzel1,2, Josef Brock2, Ralf Pöhland3, Jens Vanselow4, Wolfgang Tomek3, Falk Schneider3 and Ute Tiemann3

2 University of Rostock, Institute of Medical Biochemistry and Molecularbiology, Schillingallee 70, 18057 Rostock, Germany; 3 Unit of Reproductive Biology, Research Institute of the Biology of Farm Animals, Wilhelm-Stahl-Allee 2, 18196 Dummerstorf, Germany; and 4 Unit of Molecular Biology, Research Institute of the Biology of Farm Animals, Wilhelm-Stahl-Allee 2, 18196 Dummerstorf, Germany

Received on February 19, 2004; revised on May 25, 2004; accepted on May 25, 2004

The detection of galectin-1 (gal-1) in pig granulosa cell lysates by immunoblotting and its cytosolic as well as membrane-associated localization prompted us to study its effects on cell proliferation and regulation of progesterone synthesis. The lectin stimulated the proliferation of granulosa cells from pig ovaries cultured in serum-free medium. Gal-1 inhibited the FSH-stimulated progesterone synthesis of granulosa cells. This inhibitory effect was strongly reduced by the disaccharidic competitor lactose at 30 mM. The absence of inhibitory effects on dibutyryl-cAMP (db-cAMP), forskolin, and pregnenolone-enhanced cellular progesterone synthesis suggests that gal-1interferes with the receptor-dependent mechanism of FSH-stimulated progesterone production. In FSH-stimulated granulosa cells, western blot analysis revealed the gal-1-mediated suppression of the cytochrome P450–dependent cholesterol side chain cleavage enzyme (P450SCC) that catalyzes the conversion of cholesterol to pregnenolone. In the presence of 30 mM lactose, the gal-1-reduced P450SCC expression was prevented. Strongly reduced mRNA levels were recorded for P450SCC and 3ß-hydroxysteroid dehydrogenase/isomerase (3ß-HSD) when FSH-stimulated granulosa cells were cultured in the presence of gal-1. We conclude that gal-1 exerts its inhibitory effect on steroidogenic activity of granulosa cells by interfering the hormone–receptor interaction resulting in decreased responses to FSH stimulation.

1 To whom correspondence should be addressed; e-mail: hermann.walzel{at}med.uni-rostock.de


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