Expression of Estrogen Receptor α by Decidual Macrophages in Preeclampsia.

Polina Vishnyakova,Anastasiya Poltavets,Zulfiya Khodzhaeva,Konstantin Midiber,Alena Potapova,Liudmila Mikhaleva,Alexey Pyregov,Gennady Sukhikh,Maria Nikitina,Timur Fatkhudinov,Andrey Elchaninov,Kamilla Muminova

doi:10.3390/biomedicines9020191

Abstract

Preeclampsia is a gestation-associated hypertensive syndrome that threatens the life and health of the mother and the child. The condition is presumably caused by systemic failure with a strong involvement of innate immunity. In particular, it has been associated with flexible phenotypes of macrophages, which depend on the molecules circulating in the blood and tissue fluid, such as cytokines and hormones. This study aimed at a comparative evaluation of pro-inflammatory (TNFα) and anti-inflammatory (CD206, MMP9, HGF) markers, as well as the levels of estrogen receptor α, expressed by decidual macrophages in normal pregnancy and in patients with early- and late-onset preeclampsia. The tissue samples of decidua basalis were examined by immunohistochemistry and Western blotting. Isolation of decidual macrophages and their characterization were performed using cultural methods, flow cytometry and real-time PCR. Over 50% of the isolated decidual macrophages were positive for the pan-macrophage marker CD68. In the early-onset preeclampsia group, the levels of estrogen receptor α in decidua were significantly decreased. Furthermore, significantly decreased levels of HGF and CD206 were observed in both preeclampsia groups compared with the control group. The observed downregulation of estrogen receptor α, HGF and CD206 may contribute to the balance of pro- and anti-inflammatory macrophages and thereby to pathogenesis of preeclampsia.

Highlights

The concept of macrophage phenotype plasticity, laid down at the beginning of the20th century, was able to successfully explain the diversity of macrophage behavior, i.e., why macrophages may either behave as pro-inflammatory cells, or help to resolve inflammation and support tissue regeneration
Preeclampsia (PE), one of the so-called “great obstetrical syndromes” [1], is a gestation-associated multisystem disorder which affects from 5% to 7% of all pregnant women and leads to over 70,000 maternal and 500,000 fetal deaths per year around the world [2]
One of the hypotheses on PE etiology is a shift in the balance of pro- and anti-inflammatory macrophages within decidua basalis [3]

Summary

Introduction

The concept of macrophage phenotype plasticity, laid down at the beginning of the20th century, was able to successfully explain the diversity of macrophage behavior, i.e., why macrophages may either behave as pro-inflammatory cells, or help to resolve inflammation and support tissue regeneration. The concept of macrophage phenotype plasticity, laid down at the beginning of the. Abnormal regulation of macrophage plasticity has been increasingly considered causative for a number of pathological conditions. Preeclampsia (PE), one of the so-called “great obstetrical syndromes” [1], is a gestation-associated multisystem disorder which affects from 5% to 7% of all pregnant women and leads to over 70,000 maternal and 500,000 fetal deaths per year around the world [2]. PE is characterized by high maternal blood pressure combined with proteinuria and/or other manifestations. One of the hypotheses on PE etiology is a shift in the balance of pro- and anti-inflammatory macrophages within decidua basalis [3]. One of the hypotheses on PE etiology is a shift in the balance of pro- and anti-inflammatory macrophages within decidua basalis [3]. 4.0/).

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