Logo Logo
Hilfe
Hilfe
Switch Language to English

Freitag, Nancy; Tirado-Gonzalez, Irene; Barrientos, Gabriela; Cohen, Marie; Daher, Silvia; Goldman-Wohl, Debra; Mincheva-Nilsson, Lucia; John, Constance M.; Jeschke, Udo und Blois, Sandra M. (2020): The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus. In: American Journal of Reproductive Immunology, Bd. 84, Nr. 6, e13311

Volltext auf 'Open Access LMU' nicht verfügbar.

Abstract

Problem From conception, a delicate regulation of galectins, a family of carbohydrate-binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin-3 (gal-3), the only chimera-type galectin, is abundantly expressed at the feto-maternal interface;the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation. Method of study In this study, we analyzed serum gal-3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal-3 exogenous stimulation using trophoblastic cell lines (e.g. , HIPEC65, SGHPL-4, and BeWo cells). Finally, we investigated variations in peripheral gal-3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM). Results Gal-3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal-3 positively regulated trophoblast functions inducing invasion, tube formation, and fusion. Compared with normal pregnant women, circulating gal-3 levels were significantly decreased in patients who developed GDM. Conclusion Our results reveal a physiological role for gal-3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal-3 levels late in gestation. Thus, dysregulation of gal-3 may indicate a contribution of the chimera-type lectin to this adverse pregnancy outcome.

Dokument bearbeiten Dokument bearbeiten