GEO series

A Trisomy 21 Lung Cell Atlas

GSE272470 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2024/08/15 Platform GPL24676

Summary

Trisomy 21 (T21), resulting in Down Syndrome (DS), is the most prevalent chromosomal abnormality worldwide. While pulmonary disease is a major cause of morbidity and mortality in DS, the ontogeny of pulmonary complications remains poorly understood. We recently demonstrated that T21 lung anomalies, including airway branching and vascular lymphatic abnormalities, are initiated in utero. Here, we aimed to describe molecular changes at the single cell level in prenatal T21 lungs. Our results demonstrate differences in the proportion of cell populations and detail changes in gene expression at the time of initiation of histopathological abnormalities. Notably, we identify shifts in the distribution of alveolar epithelial progenitors, widespread induction of key extracellular matrix molecules in mesenchymal cells and hyper-activation of IFN signaling in endothelial cells. This single cell atlas of T21 lungs greatly expands our understanding of antecedents to pulmonary complications and should facilitate efforts to mitigate respiratory disease in DS.

Published in

Alterations in Resident Immune Cells in Prenatal Trisomy 21 Lungs

Frauenpreis A, Bhattacharya S, Belgacemi R et al. · Cells 2025 · PMID 41369355 · doi:10.3390/cells14231866

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Direct links to NCBI, no account and no request form: the whole study as GSE272470_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 9 samples. Raw sequencing reads are also available from ENA.

Whole study · RAW.tar ↓ Series matrix ↓ All supplementary files ↗ Raw reads on ENA ↗

Also filed as BioProject PRJNA1136930 and SRA study SRP520558. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41369355) ↗

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