Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

The Chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus

[img]
Preview
PDF (Original Article) - Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
1MB

Item Type:Article
Title:The Chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
Creators Name:Freitag, N. and Tirado-González, I. and Barrientos, G. and Cohen, M. and Daher, S. and Goldman-Wohl, D. and Mincheva-Nilsson, L. and John, C. and Jeschke, U. and Blois, S.M.
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.
Keywords:gal-3, Placenta, Trophoblast, Pathological Pregnancy
Source:American Journal of Reproductive Immunology
ISSN:1046-7408
Publisher:Wiley
Volume:84
Number:6
Page Range:e13311
Date:December 2020
Official Publication:https://doi.org/10.1111/aji.13311
PubMed:View item in PubMed

Repository Staff Only: item control page

Downloads

Downloads per month over past year

Open Access
MDC Library