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Related Experiment Video

Updated: Jun 5, 2025

Mouse Fetal Whole Intestine Culture System for Ex Vivo Manipulation of Signaling Pathways and Three-dimensional Live Imaging of Villus Development
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RANK drives structured intestinal epithelial expansion during pregnancy.

Masahiro Onji1,2, Verena Sigl3, Thomas Lendl4

  • 1Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Vienna, Austria. masahiro.onji@meduniwien.ac.at.

Nature
|December 5, 2024
PubMed
Summary
This summary is machine-generated.

Pregnancy and lactation cause intestinal expansion in mammals via the RANK-RANKL pathway, increasing surface area. This essential remodeling ensures maternal and offspring health, impacting offspring development.

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Area of Science:

  • Reproductive biology
  • Gastroenterology
  • Cellular and molecular biology

Background:

  • Mammalian reproduction involves significant physiological adaptations for maternal and offspring well-being.
  • The intestinal epithelium's role in these adaptations, particularly during pregnancy and lactation, remains incompletely understood.

Purpose of the Study:

  • To investigate the molecular mechanisms driving intestinal epithelial expansion during mammalian pregnancy and lactation.
  • To identify key pathways regulating villous morphology and intestinal surface area during reproduction.

Main Methods:

  • In vivo studies using mice, including genetic manipulation (Rank deficiency).
  • In vitro studies using mouse and human intestinal organoids.
  • Analysis of molecular signaling pathways, including Receptor activator of nuclear factor-κB (RANK) and Bone Morphogenetic Protein (BMP) signaling.

Main Results:

  • The intestinal epithelium expands during pregnancy and lactation, characterized by novel villous geometry.
  • The RANK-RANKL pathway is identified as a critical regulator of this expansion in mice and organoids.
  • RANK-RANKL signaling protects gut epithelial cells, influences the stem cell niche via BMP signaling, and promotes villous elongation.
  • Maternal deficiency in intestinal RANK leads to reduced offspring weight and glucose intolerance.
  • Constitutive RANK activation causes intestinal expansion followed by villous and stem cell loss, and inhibits tumor formation.

Conclusions:

  • RANK-RANKL is a key pathway driving intestinal epithelial expansion during pregnancy and lactation, a fundamental reproductive adaptation.
  • This pathway is crucial for maintaining gut integrity and supporting offspring development, with implications for metabolic health.
  • Understanding RANK-RANKL's role offers insights into tissue remodeling, stem cell regulation, and potential therapeutic targets.