Identification of Intercellular Crosstalk between Decidual Cells and Niche Cells in Mice.

Jia-Peng He,Qing Tian,Ji-Long Liu,Qiu-Yang Zhu

doi:10.3390/ijms22147696

Jia-Peng He, Qing Tian + Show 2 more

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https://doi.org/10.3390/ijms22147696

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Abstract

Decidualization is a crucial step for human reproduction, which is a prerequisite for embryo implantation, placentation and pregnancy maintenance. Despite rapid advances over recent years, the molecular mechanism underlying decidualization remains poorly understood. Here, we used the mouse as an animal model and generated a single-cell transcriptomic atlas of a mouse uterus during decidualization. By analyzing the undecidualized inter-implantation site of the uterus as a control, we were able to identify global gene expression changes associated with decidualization in each cell type. Additionally, we identified intercellular crosstalk between decidual cells and niche cells, including immune cells, endothelial cells and trophoblast cells. Our data provide a valuable resource for deciphering the molecular mechanism underlying decidualization.

Highlights

Decidualization is a crucial step for human reproduction
Uterine stromal cells change into large epithelioid cells and secrete two protein markers, decidual prolactin and insulin-like growth factor-binding protein 1 (IGFBP1) [3]
We identified 21 distinct cell clusters in mouse uterus during decidualization, including 5 stromal cell clusters, 2 epithelial cell clusters, 1 smooth muscle cell cluster, 1 pericyte cluster, 4 endothelial cell clusters and 8 immune cell clusters

Summary

Introduction

Decidualization is a crucial step for human reproduction. It is a prerequisite for embryo implantation, placentation and pregnancy maintenance [1]. Decidualization initiates spontaneously in the secretory phase of the menstrual cycle, which is tightly controlled by ovarian estrogen and progesterone [2]. Uterine stromal cells change into large epithelioid cells and secrete two protein markers, decidual prolactin (dPRL) and insulin-like growth factor-binding protein 1 (IGFBP1) [3]. Impaired decidualization may lead to intrauterine growth restriction (IUGR), repeated pregnancy loss (RPL) and severe pre-eclampsia (sPE) [4]. It is imperative to understand the molecular mechanism of decidualization

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