# Aryl Hydrocarbon Receptor (AHR) is required for repopulation of decellularized intestinal colon scaffolds

**Authors:** Lizbeth Perez-Castro, Busola Alabi, Afshan Nawas, M.Carmen Lafita-Navarro, Jerry Shay, Maralice Conacci-Sorrell

PMC · DOI: 10.17912/micropub.biology.001529 · 2025-04-25

## TL;DR

This study shows that the AHR protein is essential for regrowing the intestinal lining using decellularized scaffolds.

## Contribution

The study reveals a novel role for AHR in intestinal regeneration using decellularized scaffolds.

## Key findings

- Silencing AHR prevents colonic cells from repopulating decellularized colons.
- AHR's ligand-dependent activity could be targeted to treat intestinal disorders.
- AHR is critical for regulating intestinal tissue renewal.

## Abstract

This study investigates the role of the ligand-activated transcription factor AHR in repopulating the intestinal lining. Using organoid-derived cells and decellularized mouse intestinal scaffolds to investigate the importance of AHR in regulating intestinal regeneration, we found that silencing AHR expression hinders the capacity of colonic cells to repopulate decellularized colons. We therefore propose that AHR may play an important role in regulating intestinal regeneration. The ligand-dependent nature of AHR activity may provide an opportunity to interfere with disorders such as cancer and inflammatory bowel diseases which are caused by dysregulation in intestinal tissue renewal.

## Linked entities

- **Genes:** AHR (aryl hydrocarbon receptor) [NCBI Gene 196]
- **Proteins:** AHR (aryl hydrocarbon receptor)
- **Diseases:** cancer (MONDO:0004992)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Ahr (aryl-hydrocarbon receptor) [NCBI Gene 11622] {aka Ah, Ahh, Ahre, In, bHLHe76}
- **Diseases:** cancer (MESH:D009369), inflammatory bowel diseases (MESH:D015212)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12062895/full.md

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Source: https://tomesphere.com/paper/PMC12062895