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Surgical Models of Gastroesophageal Reflux with Mice

Surgical Models of Gastroesophageal Reflux with Mice

Published on: August 25, 2015

A new mouse model for studying EGFR-dependent gastric polyps.

Maik Dahlhoff¹, Markus Gerhard, Roland Rad

¹Institute of Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis, Gene Center, LMU Munich, Munich, Germany.

Biochimica Et Biophysica Acta

|May 15, 2012

Summary

Overexpression of betacellulin (BTC), an epidermal growth factor receptor (EGFR) ligand, causes severe gastric hyperplasia in mice. This finding establishes a new model for studying EGFR-dependent gastric polyps.

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Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration

Published on: May 7, 2018

Area of Science:

Gastroenterology
Molecular Biology
Oncology

Background:

Hyperactivation of epidermal growth factor receptor (EGFR) by transforming growth factor-alpha (TGFA) is linked to gastric hyperplastic lesions.
The role of other EGFR ligands in stomach diseases remains largely unexplored.

Purpose of the Study:

To investigate the effect of betacellulin (BTC) overexpression on gastric epithelium.
To establish a novel mouse model for studying EGFR-dependent gastric pathologies.

Main Methods:

Generation of transgenic mice overexpressing BTC.
Analysis of gastric morphology, cell composition, and weight in BTC transgenic mice.
Evaluation of EGFR dependency by crossing BTC transgenic mice with EGFR mutant mice.
Assessment of hormonal and androgen influences on gastric hyperplasia.

Main Results:

BTC overexpression induced severe, age-dependent gastric hyperplasia, characterized by foveolar epithelium expansion and depletion of corpus mucosa.
Gastric lesions were more pronounced in males and partially regressed after castration.
The phenotype was dependent on functional EGFR signaling, as confirmed by crossing with EGFR mutant mice.
BTC-tg mice exhibited significantly increased stomach weight (up to 10% of body weight).

Conclusions:

Betacellulin (BTC) is identified as an EGFR ligand capable of inducing severe gastric hyperplasia.
BTC-overexpressing transgenic mice represent a valuable new model for investigating EGFR-driven gastric polyps and Ménétrier's disease.
This study highlights the critical role of specific EGFR ligands in regulating gastric homeostasis.