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Galectin-3 deficiency in pregnancy increases the risk of fetal growth restriction (FGR) via placental insufficiency.

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Item Type:Article
Title:Galectin-3 deficiency in pregnancy increases the risk of fetal growth restriction (FGR) via placental insufficiency.
Creators Name:Freitag, N. and Tirado-Gonzalez, I. and Barrientos, G. and Powell, K.L. and Boehm-Sturm, P. and Koch, S.P. and Hecher, K. and Staff, A.C. and Arck, P.C. and Diemert, A. and Blois, S.M.
Abstract:Fetal growth restriction (FGR) is the most common pregnancy complication in developed countries. Pregnancies affected by FGR, frequently concur with complications and high risk of neonatal morbidity and mortality. To date, no approved treatment is available for pregnant women affected with FGR. The objective of this study was to investigate the contribution of galectin-3 (gal-3), a β-galactoside binding protein involved in pregnancy, placental function and fetal growth. We demonstrated that lack of gal-3 during mouse pregnancy leads to placental dysfunction and drives FGR in the absence of a maternal preeclampsia syndrome. Analysis of gal-3 deficient dams revealed placental inflammation and malperfusion, as well as uterine natural killer cell infiltration with aberrant activation. Our results also show that FGR is associated with a failure to increase maternal circulating gal-3 levels during the second and third trimester in human pregnancies. Placentas from human pregnancies affected by FGR displayed lower gal-3 expression, which correlated with placental dysfunction. These data highlight the importance of gal-3 in the promotion of proper placental function, as its absence leads to placental disease and subsequent FGR.
Keywords:Fetal Development, Fetal Growth Retardation, Galectin 3, Inbred C57BL Mice, Placental Insufficiency, Placentation, Pregnancy, Risk Factors, Animals, Mice
Source:Cell Death & Disease
ISSN:2041-4889
Publisher:Nature Publishing Group
Volume:11
Number:7
Page Range:560
Date:23 July 2020
Official Publication:https://doi.org/10.1038/s41419-020-02791-5
PubMed:View item in PubMed

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