Growth regulation of normal rabbit gastric epithelial cells in primary culture

利用兔胃上皮细胞原代培养体系，研究正常胃上皮细胞的生长调控机制。我们的研究结果如下：1。兔胃上皮细胞的生长受EGF、TGF α、胰岛素和cAMP的正调控，而受TGF β的负调控。2. 原癌基因，如c-fos和c-myc，是由这些生长因子诱导的，诱导程度是否与这些生长调节剂对细胞生长的影响无关。3. 尽管rhese细胞具有P2嘌呤能受体，但无论是否存在EGF.4， ATP对细胞生长都没有任何影响。与EGF、TGF α和胰岛素相比，肝细胞生长因子（HGF）是兔胃上皮细胞增殖和迁移的最有效刺激物。5. 原代培养兔胃成纤维细胞的条件培养基刺激上皮细胞的生长和迁移，抗兔HGF.6抑制上皮细胞的生长和迁移。结合实验显示HGF与胃上皮细胞特异性结合。Northern blot分析证实HGF特异性受体c-met mRNA在胃上皮细胞中表达，而在成纤维细胞中不表达。7. 胃成纤维细胞中检测到HGF mRNA的表达，而上皮细胞中未检测到。8. 在人胃溃疡组织中检测到HGF蛋白和mRNA的表达。这些结果提示生长因子调节胃上皮细胞的生长，但c-fos和c-myc的表达不是必需的，HGF可能是胃粘膜修复的重要因子。

We investigated the mechanism of the growth regulation of normal gastric epithelial cells using primary culture system of rabbit gastric epithelial cells. Results of our research were as follows : 1. Growth of rabbit gastric epithelial cells was positively regulated by EGF,TGF alpha, insulin, and cAMP,while it was negatively regulated by TGF beta. 2. Proto-oncogenes, such as c-fos and c-myc, were induced by these growth factors, whether the extent of induction was not necessary correlated with the effects of these growth regulators on cell growth. 3. Although rhese cells possessed P2 purinergic receptors, ATP did not have any effects on cellgrowth with or without EGF.4. Hepatocyte growth factor (HGF) was the most potent stimulant of rabbit gastric epithelial proliferation and migration, compared with EGF,TGF alpha, and insulin. 5. Conditioned medium of rabbit gastric fibroblasts in primary culture stimulated growth and migration of epithelial cells, which was blocked by anti-rabbit HGF.6. A binding assay revealed specific binding of HGF on gastric epithelial cells. Northern blot analysis confirmed expression of the HGF specific receptor, c-met mRNA,in gastric epithelial cells but not in fibroblasts. 7. Expression of HGF mRNA was detected in gastric fibroblasts but not in epithelial cells. 8. Expression of HGF protein and mRNA was detected in human gastric ulcers.These results suggest that growth factors regulte the growth of gastric epithelial cells, though expression of c-fos and c-myc is not essential, and that HGF might be an important factor of the repair of the gastric mucosa.