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Spatially resolved maternal and fetal cell contributions to severe Preeclampsia

GSE319236 Homo sapiens Expression profiling by high throughput sequencing; Other 152 samples Submitted 2026/06/11 Platform GPL24676
Summary
The molecular and cellular pathophysiology of the maternal-fetal interface in preeclamsia remains poorly understood, but it is increasingly clear that both mother and fetus make independent contributions to it. Here, we spatially distinguish these contributions to the severe form of the disease, per tissue and cell type, in its Early and Late presentations in gestation. In addition to concerted hypoxia, angiogenic imbalance, fibrosis and aberrant metabolism in the placenta, new maternal immune signatures, including changes in macrophages, mitochondrial dysfunction and interferon signalling in the placenta, myometrium or choreamniotic membranes, offer an explanation to systemic inflammation and endothelial dysfunction in the mother. These tissue and cell-specific responses are potential targets for therapy, with their prompt consideration in Early gestational disease likely most beneficial.
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Direct links to NCBI, no account and no request form: the whole study as GSE319236_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 152 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1422653 and SRA study SRP676562. Searching any of these in the dataset finder brings you back here.

Study design
35 conditions, each sampled once — no replicated groups
FVQ-PVBP ×2 FCM-PVBP ×2 FRH-PVBP ×2 FRK-PVBP ×2 FGS-PVBP ×2

Read from the first 40 of 152 sample titles: 35 distinct titles with little repetition. Check it against the sample list below before relying on it.

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