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Elevated expression of galectin-3, thioredoxin and thioredoxin interacting protein in preeclampsia

Authors :
Yael Einbinder
Tal Biron-Shental
Ishai Heusler
Debora Kidron
Avivit Weisz
Sydney Benchetrit
Keren Cohen-Hagai
Tali Zitman-Gal
Aliza Amiel
Gil Shechter-Maor
Sivan Farladansky-Gershnabel
Source :
Pregnancy hypertension. 26
Publication Year :
2021

Abstract

Objectives Preeclampsia (PE) is a pregnancy-related syndrome characterized by the onset of hypertension and proteinuria that can lead to end-organ dysfunction. Galectin-3 (Gal-3) is involved in cell growth, differentiation, inflammation and fibrosis. Thioredoxin (TXN) acts as antioxidant enzyme in several cellular processes, regulating inflammation and inhibiting apoptosis. TXNIP is an endogenous inhibitor of TXN. We evaluated changes in the inflammatory response of Gal-3, TXN, and TXNIP at the level of maternal blood, placenta, and umbilical cord blood of women with PE. Study design Ten women with PE and 20 with normal pregnancy (NP) were recruited during admission for delivery. Blood samples were obtained from parturients and umbilical cords, and placental tissue for analysis. Results Gal-3 and TXNIP mRNA expression were higher in maternal plasma in PE group compared to NP and were lower in cord blood plasma and placentas in the PE group. In the PE group, TXN/TXNIP mRNA ratio was higher in cord blood plasma (2.07) compared to maternal plasma (1.09). TXN/TXNIP placental protein ratio was similar between PE (0.89) and NP (0.79). ELISA demonstrated that Gal-3 levels in maternal serum were significantly higher in the PE vs. the NP group. Conclusions Pro-inflammatory changes were expressed by high Gal-3 and TXNIP mRNA in maternal blood of PE women, but not in their placental and cord blood samples. These findings may imply that the placenta has a role in protecting the fetus from the damages of inflammatory response, which is more common in PE than in NP.

Details

ISSN :
22107797
Volume :
26
Database :
OpenAIRE
Journal :
Pregnancy hypertension
Accession number :
edsair.doi.dedup.....dd94b6376fd03b0bab333840e411947e