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Updated: Jun 16, 2026
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A Quantitative Cell Migration Assay for Murine Enteric Neural Progenitors
Published on: September 18, 2013
Vitamin A facilitates enteric nervous system precursor migration by reducing Pten accumulation.
Ming Fu1, Yoshiharu Sato, Ariel Lyons-Warren
1Department of Pediatrics, Washington University School of Medicine, St Louis, MO 63110, USA.
Development (Cambridge, England)
|January 30, 2010
Summary
Vitamin A deficiency is a risk factor for Hirschsprung disease, a disorder of the enteric nervous system. Optimizing maternal nutrition may prevent some cases by supporting nerve cell development.
Area of Science:
- Developmental biology
- Neuroscience
- Genetics
Background:
- Hirschsprung disease (HSCR) results from failed enteric nervous system (ENS) precursor cell migration.
- Understanding factors influencing ENS development is critical for HSCR research.
Purpose of the Study:
- To investigate the role of retinoic acid (RA) in ENS precursor cell migration.
- To determine if vitamin A deficiency impacts HSCR development.
Main Methods:
- Utilized serum retinol-binding-protein-deficient (Rbp4(-/-)) mice with vitamin A deficiency.
- Examined the effects of retinoic acid (RA) on GDNF-induced migration, cell polarization, and lamellipodia formation.
- Assessed the impact of retinoic acid (RA) and Pten levels on ENS precursor migration.
Main Results:
- Retinoic acid (RA) is essential for GDNF-induced ENS precursor migration, polarization, and lamellipodia formation.
- Vitamin A depletion in Rbp4(-/-) mice led to distal bowel aganglionosis.
- Ret heterozygosity exacerbated vitamin A deficiency-induced aganglionosis.
- RA reduced Pten accumulation, while Pten overexpression inhibited ENS precursor migration.
Conclusions:
- Vitamin A deficiency acts as a non-genetic risk factor, increasing Hirschsprung disease penetrance and severity.
- These findings suggest that maternal nutrition optimization could be a preventative strategy for Hirschsprung disease.
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