Kinoshita Y, Nakata H, Kishi K, Kawanami C, Sawada M, Chiba T
Department of Internal Medicine, Kobe University School of Medicine, Japan.
Gastroenterology. 1998 Jul;115(1):93-100. doi: 10.1016/s0016-5085(98)70369-5.
BACKGROUND & AIMS: Gastrin stimulates acid secretion from parietal cells and histamine release from enterochromaffin-like (ECL) cells through identical gastrin receptors. However, gastrin has been shown to have a trophic effect only on ECL cells. The aim of this study was to compare gastrin-induced signal transduction pathways in the ECL and parietal cells of Mastomys natalensis, an African rodent.
Both ECL and parietal cells were isolated from the gastric mucosa of M. natalensis, and intracellular signal transduction events in response to gastrin were investigated.
Gastrin elicited histamine release from ECL cells and acid secretion from parietal cells in association with enhanced inositol phospholipid turnover. Although gastrin increased [3H]thymidine incorporation into ECL cells, it had no effect on parietal cells. Moreover, tyrosine phosphorylation and activation of mitogen-activated protein (MAP) kinase as well as c-fos and c-jun gene expression were augmented only in ECL cells. In addition, gastrin increased the formation of guanosine triphosphate-Ras with a simultaneous decrease in guanosine diphosphate-Ras levels in ECL but not in parietal cells.
Although gastrin receptors are present in both ECL and parietal cells, they activate the Ras-MAP kinase pathway only in ECL cells.
