studies on Proliferation and Differenntiation of Fibroblast in Gastric Mucosa by HElicobacter pylori infection

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To clcrnfy the mechanism of the myofibroblast proliferation, the binding sites of basic fibroblast growth factor (bFGF), plactietet-derived growth factor (PDGF), endothelin as well as their receptor, ware investingated by autoradiogrophy and in sitill hybridization As a result, the recepters of bFGF, PDGF-BB and Endothelin-1 were found to be distributed on the mesenchymal cells in chiding fibroblasts and myofibroblasts in the control group, while in the Helicobacter pytori-in fected Mongolian gerbils the number of CS23-bFGF, anacid-stable bFGF derivative, brought about the marlced increase of the number of myofibroblasts and FGF receptors. In addition, the localization of leptin and its receptor was investingated because leptin has recently atracted attention in relation to activation of fat-storing cells. In the gastric mucos of the control Mongolian gevbils, leptin immunoreactivity was observed in the endothelial cells of the microcirabatory units. In Helicobacter phylori-infected gerbits, teptin and its receptor ware recognized in the undifferentiated mesonohymal cells and myofibroblasts.