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Updated: Jan 9, 2026

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
Published on: May 7, 2018
RAB25 modulates pit cell commitment by coordinating transforming growth factor-alpha secretion from gastric
Haengdueng Jeong1,2,3, Yura Lee1, Chanyang Uhm1
1Department of Biomedical Sciences, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Rab25 loss in the stomach increases transforming growth factor-alpha (TGFA), promoting EGFR signaling and gastric lesions. Restoring TGFA levels or blocking it ameliorates these effects, highlighting Rab25
Area of Science:
- Gastroenterology
- Cell Biology
- Molecular Biology
Background:
- Epidermal Growth Factor Receptor (EGFR) signaling regulates gastric lineage commitment.
- The source and regulation of EGFR ligands in the stomach remain unclear.
Purpose of the Study:
- To investigate the role of Rab25 in regulating EGFR signaling and gastric lineage commitment.
- To elucidate the mechanism by which Rab25 influences TGFA secretion and its impact on gastric homeostasis.
Main Methods:
- Single-cell RNA sequencing analysis of gastric epithelial cells.
- Primary mouse cell culture to study Rab25 function.
- In vivo studies using Rab25 knockout (KO) mice.
- TGFA neutralization experiments.
Main Results:
- Rab25 is highly expressed in upper corpus glands and associated with pit lineage commitment.
- Rab25 deficiency enhances TGFA secretion, leading to EGFR signaling upregulation in the pit region.
- Rab25 KO mice develop gastric lesions with foveolar hyperplasia, which are reversed by TGFA neutralization.
- Reduced RAB25 expression is observed in human Ménétrier's disease.
Conclusions:
- Rab25 plays a critical physiological role in maintaining normal gastric lineage commitment.
- Rab25 regulates TGFA secretion, thereby controlling EGFR signaling and preventing gastric lesions.
- Dysregulation of Rab25 may contribute to gastric pathologies like Ménétrier's disease.
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