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Immunostaining to Visualize Murine Enteric Nervous System Development
Published on: April 29, 2015
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Epigenetics in ENS development and Hirschsprung disease.
A Torroglosa1, M M Alves2, R M Fernández1
1Department of Genetics, Reproduction and Fetal Medicine, Institute of Biomedicine of Seville (IBIS), University Hospital Virgen del Rocío/CSIC/University of Seville, Seville, Spain; Centre for Biomedical Network Research on Rare Diseases (CIBERER), Seville, Spain.
Developmental Biology
|June 21, 2016
Summary
Hirschsprung disease (HSCR) involves the failure of enteric nervous system (ENS) progenitor cells to develop correctly. This review explores epigenetic DNA modifications crucial for ENS development and their link to HSCR onset.
Area of Science:
- Developmental biology
- Genetics
- Epigenetics
Background:
- Hirschsprung disease (HSCR) is a neurocristopathy resulting from failed enteric nervous system (ENS) development.
- ENS formation relies on neural crest cell (NCC) migration, proliferation, and differentiation within the gastrointestinal tract.
- Disruptions in ENS gene expression are implicated in HSCR pathogenesis.
Purpose of the Study:
- To review epigenetic DNA modifications involved in ENS development.
- To examine epigenetic alterations associated with the onset of Hirschsprung disease.
Main Methods:
- Literature review focusing on epigenetic mechanisms in ENS development.
- Analysis of studies linking epigenetic changes to Hirschsprung disease.
Main Results:
- Epigenetic mechanisms, including DNA modification, play a critical role in regulating ENS gene expression.
- Specific epigenetic changes are associated with the development of HSCR.
Conclusions:
- Epigenetic regulation is fundamental to normal ENS development.
- Understanding these epigenetic modifications offers insights into HSCR etiology and potential therapeutic targets.
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