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Constitutive expression of hepatocyte growth factor may maintain the sheet construction of gastric epithelial cells through facilitating actin-myosin contractile system.

Biochemical and Biophysical Research Communications

Actins, physiology, Animals, Base Sequence, CHO Cells, Cell Communication, drug effects, Cell Survival, Cells, Cultured, Cricetinae, Cytochalasin B, pharmacology, DNA Primers, Dose-Response Relationship, Drug, Epithelial Cells, Epithelium, Ethanol, Female, Gastric Mucosa, metabolism, Hepatocyte Growth Factor, biosynthesis, Humans, Kinetics, Male, Molecular Sequence Data, Myosins, Polymerase Chain Reaction, RNA, Messenger, analysis, Rabbits, Recombinant Proteins, Transfection

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      Previously, we have demonstrated that hepatocyte growth factor (HGF) plays an important role in the repair process of gastric ulcer, showing that HGF expression is specifically increased at gastric ulcer edge. In the present study, we demonstrated the constitutive expression of HGF mRNA in normal mucosa, which is as much as 0.1-1.0 attomole/micrograms total RNA. In order to evaluate the hypothesis that HGF might have some role in maintenance of gastric mucosa or prevention of injury initiation, we developed an in vitro model using rabbit gastric epithelial cell in primary culture. 1% ethanol destroys the cell to cell contact to disrupt the monolayer sheet of the cells without causing any damage to cell viability, indicating that irritants may initiate the mucosal injury. HGF remarkably prevented the disruption induced by the ethanol without eliciting proliferation or migration. This action of HGF was suppressed by actin selective inhibitor, cytochalasin B, indicating that it was mediated by an actin-myosin contractile system. In conclusion, constitutively expressed HGF may prevent the initiation of gastric epithelial disruption, which is dependent on some sort if mobile action of the cells.

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