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. Anat Rec 260:213–221, 2000. © 2000 Wiley‐Liss, Inc.

Circatidal variation in epithelial cell proliferation in the mussel digestive gland and stomach

“…The entire digestive epithelium would thus be fully replaced every month (25 days) and the period of time required for the complete replacement of the epithelium of alveolotubular units in the digestive gland of mussels would be irreconcilable with previous reports that have presumed a massive renovation of the digestive epithelium every feeding cycle, viz., twice per day in intertidal mussels (Nelson and Morton 1979). In human colorectal mucosa, the average BrdU labelling index is 77‰-110‰ (Potten et al 1992), whereas in rat gastric epithelium, it is around 150‰ (Gama et al 2000). These BrdU labelling values seem to be maximum threshold values in normal nonglandular epithelia (Bertalanffy 1962;Humme and Potten 1980;Potten et al 1992;Pawlinoski et al 1999;Gama et al 2000) and are comparable with those that we have found here in stomach epithelium.…”

“…In human colorectal mucosa, the average BrdU labelling index is 77‰-110‰ (Potten et al 1992), whereas in rat gastric epithelium, it is around 150‰ (Gama et al 2000). These BrdU labelling values seem to be maximum threshold values in normal nonglandular epithelia (Bertalanffy 1962;Humme and Potten 1980;Potten et al 1992;Pawlinoski et al 1999;Gama et al 2000) and are comparable with those that we have found here in stomach epithelium. Based on similar calculations to those reported above for digestive alveolar units, the entire renewal of duct and stomach epithelia has been concluded to last 6 months (175 days) and 3 days, respectively.…”

Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis

“…The intestinal epithelium has a high turnover rate that necessitates the apoptotic removal of cells at the end of their normal life cycle (2). In neonatal rats, the exposure to stress results in increased apoptosis in the gastric (20) and the intestinal epithelium (33). In vitro studies using the rat intestinal epithelial cell line IEC-6 demonstrated a dose-dependent effect of increasing corticosteroid levels on the induction of apoptosis (34).…”

“…The exposure to stress can result in increased epithelial apoptosis of the gastrointestinal tract (20,33). To characterize animal response to repeated asphyxia/cold stress during the study, plasma corticosterone levels were measured using RIA.…”

Intestinal Damage in Strongyloidiasis: The Imbalance Between Cell Death and Proliferation

“…The direct effect of S. stercoralis on the small bowel mucosa can be related to the secreted ecdysteroids as discussed by Genta (42) and identified in other parasitic helminths (43). This hormone is structurally similar to some metabolites of human steroids (44) from which corticosteroids are known to induce apoptosis concomitant with inhibition of cell proliferation (45,46).…”