Omics · study · 2026
Intrauterine growth restriction is associated with adaptive hematopoietic reprogramming and selective immune rewiring in monozygotic twins
Listed in NCBI GEO
Prenatal growth restriction is linked to adverse neonatal and long-term health outcomes, potentially mediated by altered fetal immune development, yet underlying epigenetic mechanisms remain incompletely understood.
Description
Monozygotic dichorionic-diamniotic twins with selective fetal growth restriction (sFGR) provide a unique human model to study environmentally driven programming independent of genetic background and shared placental vasculature.
Umbilical cord blood buffy coat samples from three sFGR-discordant and two concordant control twin pairs underwent bulk RNA sequencing and genome-wide DNA methylation profiling, followed by differential expression, pathway enrichment, hematopoietic/immune module scoring, differential methylation, and integrative transcriptomic-epigenomic analyses. Compared with concordant pairs, discordant twins showed attenuated immune and inflammatory transcriptional programs and enrichment of erythroid- and hypoxia-related pathways, consistent with adaptive hematopoiesis under stress.
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Growth-restricted co-twins displayed transcriptional asymmetry, with selective enrichment of cytotoxic lymphoid signatures despite suppression of myeloid and antigen-presenting cell-associated programs. Hypomethylated regions in growth-restricted twins were enriched for immune regulatory pathways, including T cell differentiation and leukocyte activation. At selected loci, hypomethylation coincided with increased gene expression, suggesting an epigenetic contribution to this remodeling.
These findings suggest coordinated hematopoietic and immune reprogramming at birth involving compositional and cell-intrinsic changes, highlighting how intrauterine environment may shape early immune development independent of genetic background.
Links
Get the data
- GEO FTP directory ftp.ncbi.nlm.nih.gov/geo/series/GSE347nnn/GSE347379 ↗
download · from NCBI GEO
Where it is published
- GEO accession page ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE347379 ↗
landing page · from NCBI GEO
Documentation and papers
- PRJNA1529699 ncbi.nlm.nih.gov/bioproject/PRJNA1529699 ↗
project · from NCBI GEO
Topics
- Stated by source
- Expression profiling by high throughput sequencing · Homo sapiens · Methylation profiling by high throughput sequencing
- From keywords
- Life Sciences
- Inferred from text
- DNA methylation profiling 75% · RNA sequencing 75% · Sequencing 75%
Provenance · 1 source records, 11 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| NCBI GEO | GSE347379 | 9 d ago | JSON v1 |
| Field | Assertion | Extractor | Evidence |
|---|---|---|---|
| access_level | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[field].local:field:life-sciences | mapping · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencing | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /gdstype |
| concepts[method].geo_series_type:methylation-profiling-by-high-throughput-sequencing | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /gdstype |
| concepts[method].local:method:dna-methylation-profiling | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[modality].local:modality:rna-seq | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[modality].local:modality:sequencing | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[organism].NCBITaxon:9606 | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /taxon |
| description | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /summary |
| publication_date | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| title | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /title |