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The Loss of Luteal Progesterone Production in Women Is Associated With a Galectin Switch via alpha 2,6-Sialylation of Glycoconjugates

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Title: The Loss of Luteal Progesterone Production in Women Is Associated With a Galectin Switch via alpha 2,6-Sialylation of Glycoconjugates
Authors: Nio-Kobayashi, Junko Browse this author →KAKEN DB
Boswell, Lyndsey Browse this author
Amano, Maho Browse this author
Iwanaga, Toshihiko Browse this author
Duncan, W. Colin Browse this author
Issue Date: Dec-2014
Publisher: Endocrine Society
Journal Title: Journal of clinical endocrinology & metabolism
Volume: 99
Issue: 12
Start Page: 4616
End Page: 4624
Publisher DOI: 10.1210/jc.2014-2716
PMID: 25222756
Abstract: Context: Luteal progesterone is fundamental for reproduction, but the molecular regulation of the corpus luteum (CL) in women remains unclear. Galectin-1 and galectin-3 bind to the sugar chains on cells to control key biological processes including cell function and fate. Methods: The expression and localization of LGALS1 and LGALS3 were analyzed by quantitative PCR and histochemical analysis, with special reference to alpha 2,6-sialylation of glycoconjugates in carefully dated human CL collected across the menstrual cycle and after exposure to human chorionic gonadotrophin (hCG) in vivo. The effects of hCG and prostaglandin E-2 on the expression of galectins and an alpha 2,6-sialyltransferase 1 (ST6GAL1) in granulosa lutein cells were analyzed in vitro. Results: Galectin-1 was predominantly localized to healthy granulosa lutein cells and galectin-3 was localized to macrophages and regressing granulosa lutein cells. Acute exposure to luteotrophic hormones (hCG and prostaglandin E2) up-regulated LGALS1 expression (P < .001). ST6GAL1, which catalyzes alpha 2,6-sialylation to block galectin-1 binding, increased during luteolysis (P < .05) as did LGALS3 (P < .05). Luteotrophic hormones reduced ST6GAL1 and LGALS3 in vivo (P < .05) and in vitro (P < .001). There was an inverse correlation between the expression of ST6GAL1 and HSD3B1 (P < .01) and a distinct cellular relationship among alpha 2,6-sialylation, 3 beta-hydroxysteroid dehydrogenase, and galectin expression. Conclusions: Galectin-1 is a luteotrophic factor whose binding is inhibited by alpha 2,6-sialylation in the human CL during luteolysis. ST6GAL1 and galectin-3 expression is increased during luteolysis and associated with a loss of progesterone synthesis. Luteotrophic hormones differentially regulate galectin-1 and galectin-3/alpha 2,6-sialylation in granulosa lutein cells, suggesting a novel galectin switch regulated by luteotrophic stimuli during luteolysis and luteal rescue.
Type: article (author version)
URI: http://hdl.handle.net/2115/58031
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 小林 純子

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