Expression Profiles and Possible Roles of Galectins in the Corpus Luteum
Galectins, β-galactoside binding lectins, are involved in various physiological and pathological events. The corpus luteum (CL) is a transient endocrine tissue that produces large amounts of progesterone, which is essential for a successful pregnancy, and stage-specifically expresses galectin-1 and...
Gespeichert in:
Veröffentlicht in: | Trends in Glycoscience and Glycotechnology 2016/07/25, Vol.28(162), pp.E71-E77 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng ; jpn |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Galectins, β-galactoside binding lectins, are involved in various physiological and pathological events. The corpus luteum (CL) is a transient endocrine tissue that produces large amounts of progesterone, which is essential for a successful pregnancy, and stage-specifically expresses galectin-1 and galectin-3. We herein summarized current knowledge on galectins in the CL of mice, cows, and women in order to clarify the expression profiles, regulatory mechanisms, and possible roles of galectins in the CL of different species. The regressing CL of mice contained both galectin-1 and galectin-3, suggesting an involvement of galectins in the regulation of luteolysis in mice. On the other hand, the healthy functional CL of cows and women abundantly expressed galectin-1, whereas galectin-3 was increased in the regressing CL. The expression of galectin in luteal cells is differentially regulated by known endocrine and paracrine molecules such as prolactin, luteinizing hormone, human chorionic gonadotropin, and prostaglandins E and F. Interestingly, α2,6-sialylation, which inhibit galectin-1 binding and are catalyzed by ST6GAL1, were increased in the regressing CL of all animals. These findings suggest that a "galectin switch", coordinated changes in glycans and galectins in association with luteal function, represents a conserved mechanism in the regulation of luteal function beyond species. |
---|---|
ISSN: | 0915-7352 1883-2113 |
DOI: | 10.4052/tigg.1416.1E |