Abstract
We found a new function of heat shock protein (HSP) that is maintenance of higher order structure of DNA under various stresses conditions in E. coli and predicted that the induction of HSP suppress apoptosis in gastric mucosal cells. We found that various stresses for gastric mucosa, such as ethanol, oxidative stress, acid, and NSAIDs caused apoptosis in guinea pig gastric mucosal cells in vitro. Induction of HSP by pre-treatment of cells with geranylgeranylacetone (GGA), low concentrations of ethanol, and heat shock suppressed these apoptosis.
Gastric mucosal cells have a rapid cell turnover rate in vivo. We found that gastric mucosal cells in culture undergo spontaneous and rapid apoptosis, which may represent the rapid cell turnover cycle of gastric pit cells in vivo. This spontaneous apoptosis was prevented by HSP induction caused by pre-treatment of cells with GGA, low concentrations of ethanol, and heat shock. From these observations, we consider that HSP induction in gastric mucosal cells protects cells from various stresses by inhibiting apoptosis and increasing the number of gastric mucosal cell caused by inhibition of rapid cell turnover cycle in vivo.
