Dysfunction of Decidual Macrophages Is Apotential Risk Factor in the Occurrence of Preeclampsia

Abstract

Background: 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.Methods: In our study, we used conventional expression profiling to compare the expression and function of differential genes contained in decidua parietalis of the preeclampsia and normal human. After intersecting the genes differentially expressed between preeclampsia and the control and the genes contained in the ligand receptor network, we further explored their involvement in cell-to-cell interactions using CellPhoneDB analysis. We finally used single-cell sequencing to detect interactions between decidual cells.Results: After intersecting the genes of differentially expressed between preeclampsia and the control gotten by conventional sequencing 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.Conclusions: The abnormal export function of decidual macrophages affects the function of immune cells interacting with them, thereby destroying the original immune regulation mechanism, and ultimately leading to the occurrence of preeclampsia.

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“…The only current treatment is the delivery of the placenta (Burton, Redman et al, 2019). The etiology of PE is heterogeneous and complex, and studies on PE in humans have hitherto identified endothelial dysfunction, immune dysregulation and defective decidualization as elements in the pathogenesis of this disease (Garrido-Gomez, Quiñonero et al, 2020, Ho, van Dijk et al, 2017, Lv, Tong et al, 2018, Rong, Yan et al, 2021, Zhou, Zhang et al, 2008. Animal models, particularly mice and rats, have been used to study the molecular mechanisms underlying PE (Blois, Dechend et al, 2015, Winship, Koga et al, 2015.…”