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Updated: May 21, 2026

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
Published on: May 7, 2018
Transmural pressure loading enhances gastric mucosal cell proliferation.
Hiromasa Nakamizo1, Hidekazu Suzuki, Soichiro Miura
1Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
High transmural pressure stimulates gastric mucosal cell proliferation via ERK activation and AP-1 signaling. This finding sheds light on mechanical effects on gastric cells in conditions like gastroparesis.
Area of Science:
- Gastroenterology
- Cell Biology
- Molecular Biology
Background:
- Increased stomach pressure from conditions like gastroparesis can impact gastric mucosal integrity.
- The direct cellular effects of mechanical pressure on the gastric lining are not fully understood.
Purpose of the Study:
- To investigate if transmural pressure affects gastric mucosal cell proliferation.
- To identify the intracellular signaling pathways involved in pressure-induced cell responses.
Main Methods:
- Rat gastric epithelial cells were exposed to high transmural pressures.
- Cellular proliferation, DNA synthesis, and MAP kinase activation (ERK, JNK, p38) were measured.
- Immediate early gene expression (c-fos, c-myc) and AP-1 activation were assessed.
Main Results:
- High transmural pressure (80 mmHg) significantly increased DNA synthesis and proliferation.
- Early activation of ERK kinase, but not JNK or p38, was observed.
- Pressure induced c-fos and c-myc gene expression and AP-1 activation.
Conclusions:
- Gastric mucosal cell proliferation under high pressure is linked to ERK activation.
- The induction of c-fos, c-myc, and AP-1 activation are key components of this response.
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