Immunolocalization of estrogen receptor alpha and beta in gastric epithelium and enteric neurons

Abstract

A sexual dimorphism in gastric acid secretion has been known for many years, with women secreting less acid (40%) than men. The mechanisms mediating this sex difference are unknown, but a role for estrogens is suggested from animal models. Two estrogen receptor (ER) subtypes, ER and ER , mediate genomic effects of estrogens, and mRNA for both subtypes has been detected in the rat stomach. The objective of this study was to determine the cellular distribution of ER and ER proteins in the rat stomach. ER and ER proteins were detected in nuclei of fundic parietal cells and epithelial cells in the progenitor zone. In the antrum, several cells were immunoreactive for ER in regions containing stem and neuroendocrine cell types but ER protein was not detected in antral glands. Both ER and ER proteins were expressed in enteric neurons within the nucleus and cytoplasm, with specific punctate staining for ER in cell bodies and fibers. These studies are the first to show differences between ER and ER proteins in the epithelial cellular distribution in the fundus and antrum and to detect co-expression in enteric neurons. These results suggest that estrogens may inhibit gastric acid secretion via genomic effects in fundic parietal cells through either ER subtype and in antral neuroendocrine cells via ER . Moreover, co-expression of ER and ER in enteric neurons indicates that estrogenic effects could also be mediated through neurogenic reflexes. Our findings imply that direct regulation of multiple cell types by estrogens may contribute to the modulation of gastric functions that have been recognized during the estrous cycle and between the sexes.

Identification of transcriptional regulatory elements in the human somatostatin receptor sst2 promoter and regions including estrogen response element half-site for estrogen activation

“…Each trans-acting factor is encircled with a square. and sst2 (Halmos et al 2000, Campbell-Thompson et al 2001, Dougherty et al 2006, and in rodent central nervous system the arcuate nucleus expresses more sst2 in female than male (Shimizu et al 2005, Bouyer et al 2006. Since the expression of ERs is known to increase in progressed tumors (Deroo & Korach 2006), it is expected that the increased ER proteins may lead to induce the sst2 gene expression.…”

Gastric estrogen directly induces ghrelin expression and production in the rat stomach

“…Recently, Ueyama et al (2002) clearly demonstrated that estrogen synthetase (aromatase) is expressed in gastric parietal cells of the rat stomach. Furthermore, Campbell-Thompson et al (2001) reported that ERa expression was found in the stomach mucosa of rats, and Singh et al (1997) also revealed the existence of ER mRNA and protein using Northern blot analysis and enzyme immunoassay in the human stomach mucosa. Taken together, these findings suggest that estrogen produced in the stomach regulates ghrelin gene expression.…”

Use of Acid-Suppressive Drugs and Risk of Fracture: A Meta-analysis of Observational Studies

“…23 Fourth, gastric parietal cells appear to have a potent endocrine role in secreting estrogens. [24][25][26][27] Atrophy of the gastric mucosa, observed in patients infected with CagA-positive Helicobacter pylori, 28 reduces the number of gastric parietal cells and may decrease local production of estrogens. Estrogens produced in the stomach directly induce expression and production of ghrelin, 29,30 which appears to increase bone formation by osteoblasts.…”