GEO series

Maternal cause of early-onset preeclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities

GSE287645 Homo sapiens (human) RNA-seq (gene expression) 16 samples Submitted 2025/01/27 Platform GPL23227

At a glance

RNA-seq (gene expression) · human · 16 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Homo sapiens (human)
Samples: 16 samples: 5 × organoid_NT vs 5 × organoid_PET vs 3 × tissue_NT vs 3 × tissue_PETGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalitiesJournal of biomedical science · 2025

Summary (written by the submitters)

Early-onset pre-eclampsia (ePE) is a severe pregnancy complication affecting millions of pregnancies worldwide, resulting in significant maternal and fetal morbidity. The etiology of ePE is associated with defective trophoblast functions, leading to abnormal placental development. Regulatory factors released by endometrial glands are crucial for proper placental development.

Read the full summary ↓

While circumstantial evidence indicates that defective endometrial gland development or function may lead to defective placental development and ePE in humans, direct evidence has been lacking. This study explored the role of endometrial gland-derived factors both in vitro and in vivo and correlated the findings with the clinical phenotypes of ePE. Our findings revealed that the secretome of organoids derived from the endometrial tissues of ePE patients impeded spiral artery remodeling and thus disrupted proper placental perfusion. Transcriptomic and proteomic analyses identified an increased apolipoprotein D (APOD) production in ePE organoids and decidual tissues compared to their normotensive (NT) counterparts. Overexpression of endometrial APOD impaired the vascular remodeling functions of extravillous trophoblasts (EVT) and endothelial cells in vitro. These findings were corroborated using an endometrial-specific APOD knock-in mouse model. APOD-induced ferroptosis through the PI3K/Akt pathway in both human ePE placentas and the mouse model. Moreover, elevated APOD levels were detected in the first-trimester serum of pregnant women who subsequently developed ePE. These results provide the first direct evidence that dysregulated endometrial gland secretome is a maternal cause of defective placental development and ePE. Clinically, APOD could serve as a biomarker for early detection of ePE, enabling early intervention with the potential to improve outcomes for both mothers and their babies.

Published in

Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities

Dong Y, Lee CL, Li J et al. · Journal of biomedical science 2025 · PMID 41366770 · doi:10.1186/s12929-025-01199-7

This dataset

Open GSE287645 in finder → Find more human RNA-seq datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE287645_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1213976 and SRA study SRP558925. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41366770) ↗

Study design

5 × organoid_NT vs 5 × organoid_PET vs 3 × tissue_NT vs 3 × tissue_PET

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 16 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM8749282 organoid_NT_1 organoid_NT
GSM8749283 organoid_NT_2 organoid_NT
GSM8749284 organoid_NT_3 organoid_NT
GSM8749285 organoid_NT_4 organoid_NT
GSM8749286 organoid_NT_5 organoid_NT
GSM8749287 organoid_PET_1 organoid_PET
GSM8749288 organoid_PET_2 organoid_PET
GSM8749289 organoid_PET_3 organoid_PET
GSM8749290 organoid_PET_4 organoid_PET
GSM8749291 organoid_PET_5 organoid_PET
GSM8749292 tissue_NT_1 tissue_NT
GSM8749293 tissue_NT_2 tissue_NT
GSM8749294 tissue_NT_3 tissue_NT
GSM8749295 tissue_PET_1 tissue_PET
GSM8749296 tissue_PET_2 tissue_PET
GSM8749297 tissue_PET_3 tissue_PET

Datasets on a similar topic

GSE247109 Upregulation of Siglec-6 induces mitochondrial dysfunction by promoting GPR20 expression in early-onset preeclampsia 6 samples shares preeclampsia, early-onset
GSE302952 WTAP Regulates NCOA4-Mediated Ferroptosis via a YTHDF2-Dependent Mechanism in Preeclampsia 6 samples shares preeclampsia, ferroptosis
GSE91077 Global transcriptional profiling confirmed failed decidualization of human Endometrial Stromal Cells (hESCs) obtained from non-pregnant women with a previous pregnancy complicated by severe preeclampsia (sPE). 20 samples shares preeclampsia, endometrial
GSE44711 Gene expression in Early-Onset Preeclampsia Placentas and Controls 16 samples shares preeclampsia, early-onset
GSE264073 Ileal Enterocyte Brush Border Abnormalities Associate with Progressive Disease Course in Pediatric Crohn’s Disease 152 samples shares abnormalities
GSE243579 iPSC-based modeling of preeclampsia identifies defects in extravillous trophoblast differentiation 144 samples shares preeclampsia
GSE306864 Placental transcriptome profiles in late-onset preeclampsia: a cross-sectional observational analysis stratified by fetal sex 58 samples shares preeclampsia
GSE251822 A high-fidelity CRISPR-Cas13 system improves abnormalities associated with C9ORF72-linked ALS/FTD 54 samples shares abnormalities

Search all human RNA-seq datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.