Gal-2 Increases H3K4me3 and H3K9ac in Trophoblasts and Preeclampsia

Preeclampsia (PE) is a severe pregnancy disorder with a pathophysiology not yet completely understood and without curative therapy. The histone modifications H3K4me3 and H3K9ac, as well as galectin-2 (Gal-2), are known to be decreased in PE. To gain a better understanding of the development of PE, t...

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Published inBiomolecules (Basel, Switzerland) Vol. 12; no. 5; p. 707
Main Authors Hahn, Laura, Meister, Sarah, Mannewitz, Mareike, Beyer, Susanne, Corradini, Stefanie, Hasbargen, Uwe, Mahner, Sven, Jeschke, Udo, Kolben, Thomas, Burges, Alexander
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 15.05.2022
MDPI
Subjects
Apoptosis
Binding sites
Cell culture
Cell fusion
E-cadherin
Epigenetics
Experiments
galectin-2
H3K4me3
H3K9ac
histone modification
Histones
Hypertension
Metabolism
Placenta
Polymers
Pre-eclampsia
Preeclampsia
Pregnancy
Reagents
syncytialisation
Therapeutic targets
Trophoblasts
β-Catenin
United States > US
Berlin Germany
Germany
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Summary:Preeclampsia (PE) is a severe pregnancy disorder with a pathophysiology not yet completely understood and without curative therapy. The histone modifications H3K4me3 and H3K9ac, as well as galectin-2 (Gal-2), are known to be decreased in PE. To gain a better understanding of the development of PE, the influence of Gal-2 on histone modification in trophoblasts and in syncytialisation was investigated. Immunohistochemical stains of 13 PE and 13 control placentas were correlated, followed by cell culture experiments. An analysis of H3K4me3 and H3K9ac was conducted, as well as cell fusion staining with E-cadherin and β-catenin—both after incubation with Gal-2. The expression of H3K4me3 and H3K9ac correlated significantly with the expression of Gal-2. Furthermore, we detected an increase in H3K4me3 and H3K9ac after the addition of Gal-2 to BeWo/HVT cells. Moreover, there was increased fusion of HVT cells after incubation with Gal-2. Gal-2 is associated with the histone modifications H3K4me3 and H3K9ac in trophoblasts. Furthermore, syncytialisation increased after incubation with Gal-2. Therefore, we postulate that Gal-2 stimulates syncytialisation, possibly mediated by H3K4me3 and H3K9ac. Since Gal-2, as well as H3K4me3 and H3K9ac, are decreased in PE, the induction of Gal-2 might be a promising therapeutic target.
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These authors contributed equally to this work.
ISSN:2218-273X
2218-273X
DOI:10.3390/biom12050707