Abstract
Preeclampsia is a multi-factorial and multi-genetic disorder that affects more than eight million mother and baby pairs each year. Currently, most of the attention to the pathogenesis of preeclampsia has been focused on placenta, but recent progresses suggest that excellent decidualization lays foundation for placentation and growth. Moreover, preeclampsia is associated with an imbalance in immunoregulatory mechanisms, however, how the immune regulatory system in the decidua affects preeclampsia is still unclear. In our study, after intersecting the genes of differentially expressed between preeclampsia and the control gotten by conventional expression profile analysis and the genes contained in the ligand receptor network, we found eight differentially expressed genes in a ligand-receptor relationship, and the eight genes have a characteristic: most of them participate in the interaction between decidual macrophages and other decidual immune cells. The results of single-cell sequencing of decidual cells further demonstrated that decidual macrophages affect the functions of other immune cells through export. As a result, abnormal gene expression affects the export function of decidual macrophages, which in turn affects the interaction of decidual macrophages with other immune cells, thereby destroying the original immune regulation mechanism, and ultimately leading to the occurrence of preeclampsia.
Highlights
Preeclampsia (PE) is a pregnancy-related syndrome with high blood pressure (≥ 140/90 mmHg) and/or proteinuria (≥ 0.3 g/L) [1]
Through the analysis of single-cell sequencing data, we found that ICAM1 and CXCL3 are both expressed in normal decidual macrophages (dM), but IGF1, CXCL12, NRP1, LRP6, PDGFD and PDGFRB are not expressed in normal dM, nor are they expressed in other immune cells (Figures 3, 4)
We found that most of differential genes exist in the interrelationship between decidual macrophages and other decidual immune cells
Summary
Preeclampsia (PE) is a pregnancy-related syndrome with high blood pressure (≥ 140/90 mmHg) and/or proteinuria (≥ 0.3 g/L) [1] It is a human-specific disease that can severely cause uteroplacental dysfunction, intrauterine growth restriction, and premature birth, and is one of the major causes of maternal and fetal morbidity and mortality [2]. Decidualization is a transformation that endometrial stromal cells must undergo in order to adapt to pregnancy, by affecting trophoblast invasion, embryo implantation [6]. It firstly begins near spiral artery and gradually spreads to all endometrium [7]. Aberrant frequency and function of decidual immune cells have been reported in a variety of obstetric complications, including PE, recurrent pregnancy loss, and preterm delivery [11, 12]
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