Regulation of Reg gene expression in ECL cells

我们已经发表了Reg蛋白是由大鼠胃粘膜ECL细胞产生的。在本研究中，我们研究了REG基因在大鼠胃粘膜和体外培养的ECL细胞中表达的调控机制。在病毒研究中，只有在粘膜强度保持不变的情况下，Reg基因的表达才不受胃泌素的调节。另一方面，胃黏膜损伤时，CINC-2β可增强REG基因的表达，而胃泌素对REG基因表达无明显影响。在分离的ECL细胞中，胃和CINC-2β单独刺激REG基因的表达。胃受体和CXCR1趋化因子受体表达于ECL细胞，REG受体表达于腺颈部的增殖祖细胞。我们的结果表明胃泌素对胃粘膜有刺激作用。在正常胃粘膜中表达Via Reg蛋白。在损伤的胃粘膜中，CINC-2β通过REG刺激胃粘膜的增殖。

We have already published that Reg protein is produced by ECL cells in rat gastric mucosa. In this study, we have investigated the mechanism of the control of Reg gene expression in rat gastric mucosa and in isolated rat ECL cells. In viro study, Reg gene expression was unregulated by gastrin only when the mucosal intensity was intact. On the other hand, Reg gene expression was augmented by CINC-2 β when the gastric mucosa was damaged, but rat by gastrin. In isolated perifieced ECL cells, gastric and CINC-2β independently stimulated Reg gene expression. Gastric receptor and CXCR1 chemokine receptor were found on ECL cells and Reg receptor was found on proliferating progenitor cells in gland neck zone. Our results clarified that gastrin stimulated gastric mucosa. In via Reg protein in normal gastric mucosa. In injured gastric mucosa, CINC-2β stimulated the proliferation of gastric mucosa Via Reg.