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

Cell death & disease, 2020-07, Vol.11 (7), p.560-560, Article 560 [Peer Reviewed Journal]

The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;info:eu-repo/semantics/openAccess ;The Author(s) 2020 ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/s41419-020-02791-5 ;PMID: 32703931

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Title:
Galectin-3 deficiency in pregnancy increases the risk of fetal growth restriction (FGR) via placental insufficiency
Author: Freitag, Nancy ; Tirado-Gonzalez, Irene ; Barrientos, Gabriela ; Powell, Katie L ; Boehm-Sturm, Philipp ; Koch, Stefan P ; Hecher, Kurt ; Staff, Anne C ; Arck, Petra C ; Diemert, Anke ; Blois, Sandra M
Subjects: Animals ; Cell activation ; Female ; Fetal Development ; Fetal Growth Retardation - metabolism ; Fetuses ; Galectin 3 - deficiency ; Galectin 3 - metabolism ; Galectin-3 ; Health risk assessment ; Humans ; Male ; Mice, Inbred C57BL ; Morbidity ; Natural killer cells ; Neonates ; Placenta ; Placental Insufficiency - metabolism ; Placentation ; Pre-eclampsia ; Pregnancy ; Pregnancy complications ; Risk Factors ; Uterus
Is Part Of: Cell death & disease, 2020-07, Vol.11 (7), p.560-560, Article 560
Description: 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.
Publisher: England: Springer Nature B.V
Language: English;Norwegian
Identifier: ISSN: 2041-4889
EISSN: 2041-4889
DOI: 10.1038/s41419-020-02791-5
PMID: 32703931
Source: ROAD
MEDLINE
NORA Norwegian Open Research Archives
PubMed Central
Nature (Open access)
ProQuest Central
DOAJ Directory of Open Access Journals

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

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