Cell proliferation and death in the gastric epithelium of developing rats after glucocorticoid treatments

Abstract

Glucocorticoids take part in the intense morphofunctional modifications that occur in the gastric mucosa during fetal and postnatal development. Two studies were designed to evaluate corticoids role in gastric cell proliferation and apoptosis in developing rats: in vivo, using suckling animals; in vitro, using gastric explants obtained from 20-day fetuses. These explants were cultured in DMEM/F12 medium treated or not with 50 ng/ml of corticosterone; after 22 hr, vincristine was added to the medium for 2 hr to block mitosis. The metaphasic index decreased significantly after the 24-hr treatment (controls: 1.52 +/- 0.53; treated: 0.40 +/- 0.21) and apoptotic cells were visualized under light and electron microscopy. Fifteen-day-old rats were treated with hydrocortisone (25 mg/Kg) for 3 days, and injected with BrDU (100 mg/Kg) 1 hr before sacrifice on the 18th day. BrDu-labeled and non-labeled cells were counted to determine the labeling index of epithelial cells. As apoptotic cells are rapidly eliminated, other animals were treated for only 2-3 hr. Sections were investigated for the presence of apoptotic cells, using morphological criteria and TUNEL labeling. Hydrocortisone significantly reduced the labeling index (controls: 15.6 +/- 1.6 vs. treated: 11.7 +/- 1.1), besides altering the body weight gain. Hydrocortisone treatment doubled the number of apoptotic cells after 2 hr, and quadruplicated it after 3 hr. The results demonstrated that glucocorticoids inhibit cell proliferation in the gastric epithelium of fetuses and suckling rats and increase apoptotic rates, suggesting the exit from cell cycle.

Changes of ultrastructure and downregulation of heat shock protein 70 and fibroblast growth factor 2 in gastric mucosa of rats with depressive-like behaviour

“…GC was found to be involved in physiological activities of the gastric mucosa. For instance, Gama et al treated rats in vivo and the cultured rat gastric tissue in vitro with GC, and the results showed decreased gastric epithelial cell proliferation as well as increased cell apoptosis (16). It was also found that GC could regulate the expression of MUC5AC mRNA, which directly inhibits the synthesis of epithelial mucus layer (17).…”

Lifelong Adaptation of Gastric Cell Proliferation and Mucosa Structure to Early Weaning-Induced Effects

“…Breastfeeding maintenance is essential to growth (Lin et al, 1998 ; Tang et al, 1999 ; Gama et al, 2000 ; Marion et al, 2005 ; de Andrade Sá et al, 2008 ; Osaki et al, 2010 ; Rogier et al, 2014 ; Bittar et al, 2016 ; Zulian et al, 2017 ), and its premature interruption can affect gastric development; we had two main goals in this study: (1) to evaluate whether the proliferative stimulus of early weaning would be lifelong detected and how it would be associated with the distribution of dividing cells in the gland, and (2) to identify the molecules of TGFβ cascade and cell cycle response and their behavior in the gastric mucosa after breastfeeding interruption.…”

Cytosine Arabinoside Induces Programmed Endothelial Cell Death Through the Caspase-3 Pathway

“…Administration of hydrocortisone reduced the proliferation of the gastric epithelium in rat fetuses and pups. This was associated with increased apoptosis as measured by the TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay (Gama, Goldfeder, De Moraes, & Alvares, 2000). In another study (Nittoh et al, 1998), five types of glucocorticoids were tested for their effects on the viability of eosinophils and neutrophils.…”