Regulation of Reg gene expression in ECL cells

我们已经发表了Reg蛋白由大鼠胃粘膜ECL细胞产生。在这项研究中，我们已经调查了Reg基因表达的控制机制，在大鼠胃粘膜和分离的大鼠ECL细胞。在体外研究中，只有当粘膜强度完整时，Reg基因的表达才不受胃泌素的调节。CINC-2 β可增强胃粘膜损伤后Reg基因的表达，而胃泌素可增强胃粘膜损伤后Reg基因的表达。在分离的外周ECL细胞中，胃和CINC-2β独立地刺激Reg基因表达。在ECL细胞上发现胃受体和CXCR 1趋化因子受体，在腺颈区的增殖祖细胞上发现Reg受体。结果表明，胃泌素对胃粘膜有刺激作用。在正常胃粘膜中via Reg蛋白表达。CINC-2β通过Reg.

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.