Human trophoblast requires galectin-3 for cell migration and invasion

Bojić‐Trbojević, Žanka; Krivokuća, Milica Jovanović; Vilotić, Aleksandra; Kolundžić, Nikola; Stefanoska, Ivana; Zetterberg, Fredrik; Nilsson, Ulf J.; Leffler, Hakon; Vićovac, Ljiljana

doi:10.1038/s41598-018-38374-w

Cited by 33 publications

(34 citation statements)

References 73 publications

(100 reference statements)

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“…In addition, our analysis of EVT gal‐3 expression revealed that the chimera lectin is highly expressed in the EVT layer of the human placenta. This observation is in agreement with previous studies showing that both interstitial and endovascular EVT are main sources of gal‐3 10 and with the recently established role of gal‐3 as a component of the human trophoblast invasion machinery 26 . The functional studies reported here have confirmed that gal‐3 participates in trophoblast cell migration/invasion.…”

Section: Discussionsupporting

confidence: 93%

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

Freitag

Tirado‐González

Barrientos

et al. 2020

American J Rep Immunol

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Section: Discussionsupporting

confidence: 93%

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

Freitag

Tirado‐González

Barrientos

et al. 2020

American J Rep Immunol

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“…implantation 19,20 . Subsequent studies have revealed that endometrial gal-3 is involved in embryo implantation 21 and dysregulation of placental gal-3 is associated with adverse pregnancy outcomes [12][13][14][15][16]22,23 . The present study demonstrates that gal-3 is critical for orchestrating healthy fetal-maternal interface interactions and its dysregulation results in asymmetric FGR.…”

Section: Discussionmentioning

confidence: 99%

“…Galectin-3 was initially reported to be a factor related to endometrial receptivity due to its increased expression in the endometrium and trophoblast during embryo implantation 19 , 20 . Subsequent studies have revealed that endometrial gal-3 is involved in embryo implantation 21 and dysregulation of placental gal-3 is associated with adverse pregnancy outcomes 12 – 16 , 22 , 23 . The present study demonstrates that gal-3 is critical for orchestrating healthy fetal-maternal interface interactions and its dysregulation results in asymmetric FGR.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2020

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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.

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“…In addition, LGALS3 gene (encoding galectin-3) was downregulated in trophoblasts from CZS-affected twins after ZIKV BR infection. LGALS3 is a galectin that has been described as involved in the process of trophoblast cell migration and invasion, significant for human embryo implantation [ 92 , 93 ]. Overall, downregulation of genes involved in trophoblast adaptation to the intrauterine environment, including ITGA1 , COL3A1 and LGALS3 ( S9 Fig ), in the trophoblasts of CZS-affected twins after ZIKV BR infection, may affect trophoblast migration, implantation, homeostasis and possibly impair the control of ZIKV BR infection.…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression elicited by ZIKV infection in trophoblasts from congenital Zika syndrome discordant twins

et al. 2020

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Zika virus (ZIKV) causes congenital Zika syndrome (CZS), which is characterized by fetal demise, microcephaly and other abnormalities. ZIKV in the pregnant woman circulation must cross the placental barrier that includes fetal endothelial cells and trophoblasts, in order to reach the fetus. CZS occurs in~1-40% of cases of pregnant women infected by ZIKV, suggesting that mothers' infection by ZIKV during pregnancy is not deterministic for CZS phenotype in the fetus. Therefore, other susceptibility factors might be involved, including the host genetic background. We have previously shown that in three pairs of dizygotic twins discordant for CZS, neural progenitor cells (NPCs) from the CZS-affected twins presented differential in vitro ZIKV susceptibility compared with NPCs from the non-affected. Here, we analyzed human-induced-pluripotent-stem-cell-derived (hiPSC-derived) trophoblasts from these twins and compared by RNA-Seq the trophoblasts from CZS-affected and non-affected twins. Following in vitro exposure to a Brazilian ZIKV strain (ZIKV BR), trophoblasts from CZS-affected twins were significantly more susceptible to ZIKV BR infection when compared with trophoblasts from the non-affected. Transcriptome profiling revealed no differences in gene expression levels of ZIKV candidate attachment factors, IFN receptors and IFN in the trophoblasts, either before or after ZIKV BR infection. Most importantly, ZIKV BR infection caused, only in the trophoblasts from CZS-affected twins, the downregulation of genes related to extracellular matrix organization and to leukocyte activation, which are important for trophoblast adhesion and immune response activation. In addition, only trophoblasts from non-affected twins secreted significantly increased amounts of chemokines RANTES/CCL5 and IP10 after infection with ZIKV BR. Overall, our results showed that trophoblasts from non-affected twins have the ability to more efficiently activate genes that are known to play important roles in cell adhesion and in triggering the immune response to PLOS NEGLECTED TROPICAL DISEASES

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Human trophoblast requires galectin-3 for cell migration and invasion

Cited by 33 publications

References 73 publications

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

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

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

Differential gene expression elicited by ZIKV infection in trophoblasts from congenital Zika syndrome discordant twins

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