Single-cell RNA-seq reveals developmental deficiencies in both the placentation and the decidualization in women with late-onset preeclampsia

Jing Yang; Lili Gong; Qiming Liu; Huanqiang Zhao; Zekun Wang; Xiaotian Li; Weidong Tian; Qiongjie Zhou

doi:10.3389/fimmu.2023.1142273

Single-cell RNA-seq reveals developmental deficiencies in both the placentation and the decidualization in women with late-onset preeclampsia

Front Immunol. 2023 May 22:14:1142273. doi: 10.3389/fimmu.2023.1142273. eCollection 2023.

Authors

Jing Yang¹, Lili Gong², Qiming Liu¹, Huanqiang Zhao², Zekun Wang¹, Xiaotian Li^{2

3}, Weidong Tian^{1

4

5}, Qiongjie Zhou^{2

3}

Affiliations

¹ State Key Laboratory of Genetic Engineering and Collaborative Innovation Center for Genetics and Development, Department of Computational Biology, School of Life Sciences, Fudan University, Shanghai, China.
² Obstetrics and Gynaecology Hospital, Fudan University, Shanghai, China.
³ Obstetrics and Gynecology Hospital, Key Laboratory of Female Reproductive Endocrine-Related Diseases, Fudan University, Shanghai, China.
⁴ Children's Hospital of Fudan University, Shanghai, China.
⁵ Children's Hospital of Shandong University, Jinan, Shandong, China.

Abstract

Preeclampsia (PE) is a leading cause of maternal and fetal morbidity and mortality. Although increasing lines of evidence suggest that both the placenta and the decidua likely play roles in the pathogenesis of PE, the molecular mechanism of PE remains elusive partly because of the heterogeneity nature of the maternal-fetal interface. In this study, we perform single-cell RNA-seq on the placenta and the decidual from patients with late-onset PE (LOPE) and women in normal pregnancy. Analyses of single-cell transcriptomes reveal that in LOPE, there are likely a global development deficiency of trophoblasts with impaired invasion of extravillous trophoblasts (EVT) and increased maternal immune rejection and inflammation in the placenta, while there are likely insufficient decidualization of decidual stromal cells (DSC), increased inflammation, and suppressed regulatory functions of decidual immune cells. These findings improve our understanding of the molecular mechanisms of PE.

Keywords: decidua; epithelial-mesenchymal transition; placenta; preeclampsia; single-cell RNA-seq.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Decidua / pathology
Female
Humans
Inflammation / pathology
Placentation*
Pre-Eclampsia* / pathology
Pregnancy
Single-Cell Gene Expression Analysis

Grants and funding

This study was supported by the National Key Research and Development Program (2021YFC2701600, 2021YFC2701601, 2021YFC2701602, 2021YFC2701603), the National Natural Science Foundation of China (81971411, 82101785, 82101786, 81741047, 31871325 and 32170667), Shanghai Sailing Program (21YF1403800), the Shanghai Key Program of Clinical Science and Technology Innovation (No. 17411950500, No. 17411950501 and No. 18511105602), Clinical Research Plan of SHDC (SHDC2020CR1047B and SHDC2020CR6021), the Shanghai Excellent Young Scholar Plan of Public Health (2020-2022, GWV-10.2-YQ13), Elite Young Scholar 2025 of Fudan University (2020-2023), Shanghai Medical Center of Key Programs for Female Reproductive Diseases (2017ZZ01016).