Biological modulation of the epithelial-mesenchymal interaction in gut wound repair process.

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It has been generally accepted that the epithelial-mesenchymal interaction plays an important role in gut would repair process. In this project, we investigated the detailed mechanism of action of several growth factors, cytokines, ECM, toxic agents, trace minerals and physical stress in gut would healing using in vivo and in vitro would healing model. As expected, each growth factor has its own target cells and some growth factors show their effects by paracrine and autocrine mechanism. Among these growth factors, insulin-like growth factor 1 played a key role in gastric wound healing in vivo and in vitro. In this mechanism zinc stimulated the production of insulin-like growth factor 1 from fibroblasts and endothelial cells and induced insulin-like growth factor 1 affected to gastric epithelial cell migration and proliferation. In another series of experiments, we showed that heat shock protein 72 has cytoprotective effect in the stomach and pre-induction of heat shock protein 72 prevented gastric mucosal damage in the several experimental model with rats. In the experiment using strain stress in vitro, heat shock protein 72 was found in decreased significantly in the gastric epithelial cells and strain stress also inhibited gastric epithelial migration and proliferation resulting in the delay of wound healing. In the clinical situation, we found the inhibition of the heat shock protein expression in the Helicobacter pylori infected gastric mucosa. Therefore heat shock protein as well as growth factors may play an important role in the integrity of gastric mucosal damage and wound healing.