Effect of acute and chronic glucocorticoid treatments on epithelial cell proliferation in the esophagus and small intestine of rats

Abstract

Data about glucocorticoid influence on proliferation in the esophagus and small intestine are very contradictory and need to be reexamined. Moreover, only the effects of acute or short-term treatments with glucocorticoids have been demonstrated, whereas nothing is known about their effects under chronic exposure. This work was therefore carried out to examine proliferative activity in the esophagus and small intestine under conditions of acute and chronic glucocorticoid exposure. Rats were treated with either glucocorticoid triamcinolone acetonide or vehicle for 3, 33, or 63 days. Proliferation was assessed in the basal layer of esophageal epithelium and in the epithelium of jejunal crypts, using three criteria, as the number of mitotic, bromodeoxyuridine-labelled, and proliferating cell nuclear antigen-labelled cells. Treatment with glucocorticoid for 3 days led to a slight decrease in all parameters in the esophageal epithelium and had almost no effect on proliferation in the epithelium of jejunal crypts. Long-term treatment with glucocorticoid for either 33 or 63 days resulted in an increase in all parameters tested in both esophageal and jejunal crypt epithelia. Sixty-three-day treatment had a more prominent and significant (P < 0.05) effect. These results suggest that acute glucocorticoid treatment nonsignificantly reduces the number of cells in the cell cycle in the esophageal epithelium, whereas chronic treatment increases the number of proliferating cells in both esophageal and jejunal crypt epithelia.

Histochemical Analyses of Altered Fetal Lung Development Following Single vs Multiple Courses of Antenatal Steroids

“…The arrested alveolarization in CRH-null mice is associated with diminished mesenchymal cell proliferation at embryonic day (E)16.5, then diminished epithelial cell differentiation plus elevated epithelial cell proliferation at E18.5; all of these abnormalities can be completely corrected by treatment with Dex in utero (Muglia et al 1995). Similar to our observations, glucocorticoids also have been demonstrated to induce cell proliferation in both in vitro and in vivo systems (Emanuel et al 1999;Gunin and Nikolaev 1999).…”

Differential expression of glucocorticoid receptor in carcinomas of the human digestive system

“…Taken together, these observations strongly suggest that GCs and GR play roles in the pathobiology of oesophageal squamous epithelia. In fact, it has been shown in rat oesophageal epithelia that short‐term GC treatment reduces the number of cells in the cell cycle, whereas chronic treatment increases the number of proliferating cells 34 . Furthermore, epidemiological evidence suggests the potential involvement of GCs in the development of oesophageal hyperplasia and cancer 35 .…”

“…treatment increases the number of proliferating cells. 34 Furthermore, epidemiological evidence suggests the potential involvement of GCs in the development of oesophageal hyperplasia and cancer. 35 The strong expression of GR in HCC and oesophageal SCC also raises concerns about the potential influence of the widespread use of GCs in combination with antineoplastic agents in the clinical management of patients with these carcinomas.…”

Intestinal Development in Neonatal Calves: Effects of Glucocorticoids and Dependence on Colostrum Feeding¹

“…Thus, formula-feeding might result in reduced maturation of the intestinal mucosa in the neonate, and glucocorticoids may, under these conditions, stimulate cell proliferation. Moreover, in neonates of altricial species with an immature GIT, glucocorticoids affect cell proliferation up to 2 months after birth [2,42].…”