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Updated: Jun 13, 2026

Recapitulating Suckling-to-Weaning Transition In Vitro using Fetal Intestinal Organoids
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Published on: November 15, 2019

Intra-Abdominal Bowel Dilation in Experimental Gastroschisis is Associated with a Modifiable Transcriptomic Program

Mary Elizabeth Guerra, Tomohiro Arai, Luc Joyeux

    Biorxiv : the Preprint Server for Biology
    |June 12, 2026
    PubMed
    Summary

    Gastroschisis causes intestinal dysfunction and dilation, with gene expression changes worsening over time. Prenatal repair in a fetal model normalized bowel dilation and gene expression, supporting early intervention.

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    Published on: June 24, 2020

    Area of Science:

    • Fetal surgery
    • Genomics
    • Neonatal surgery

    Background:

    • Gastroschisis leads to significant intestinal dysfunction and poor outcomes, often linked to intra-abdominal bowel dilation.
    • Genome-wide transcriptional profiles in gastroschisis, especially concerning disease severity, are not well understood.
    • Existing research implicates inflammation and neurovascular impairment, but lacks comprehensive gene expression data.

    Purpose of the Study:

    • To characterize intestinal transcriptional profiles in gastroschisis.
    • To analyze the temporal evolution of these transcriptional changes.
    • To assess the impact of fetal intervention on gastroschisis-associated intestinal dysfunction.

    Main Methods:

    • Utilized a fetal ovine model of complex gastroschisis with significant intra-abdominal bowel dilation.
    • Performed bulk RNA sequencing on proximal small intestinal tissue from mid-gestation and term fetuses.
    • Analyzed differential gene expression and pathway enrichment, focusing on ECM, ENS, angiogenic, and inflammatory pathways.

    Main Results:

    • Gastroschisis intestine showed minimal transcriptional differences at mid-gestation but substantial dysregulation (2,423 DEGs) by term, paralleling progressive bowel dilation.
    • Normal intestinal maturation patterns were altered, with early ECM pathway aberrations and later dysregulation of ENS, angiogenic, and inflammatory pathways.
    • Prenatal repair significantly normalized gene expression at term (29 DEGs vs. controls), alongside reduced bowel dilation.

    Conclusions:

    • Intestinal transcriptional changes in gastroschisis correlate with progressive bowel dilation, suggesting a role for mechanical stress in intestinal injury.
    • Prenatal repair effectively normalizes both intestinal dilation and associated gene expression patterns.
    • These findings support the rationale for early fetal intervention in gastroschisis to modify the transcriptional program and improve outcomes.