Endometrial responses to a deciduogenic stimulus in ovariectomized rhesus monkeys treated with oestrogen and progesterone

Abstract

ABSTRACT To establish an artificial model for the study of decidual cell reaction in the rhesus monkey, long-term ovariectomized animals were treated with oestrogen followed by progesterone and an artificial deciduogenic stimulus was applied on day 16 of the treatment cycle. Histological examinations of the endometrial samples on different days following stimulation showed prominent epithelial plaque reaction by day 20. Marked subepithelial oedema surrounding plaque cells was also noted. On day 32, degenerating plaque cells with leucocytic infiltration were found. Beginning on day 24 of hormone treatment, stromal fibroblasts adjacent to plaque and glands showed swelling with rounding-up and enlargement of nuclei; these stromal cells appeared more decidual-like with moderate amounts of hypertrophy and few were binucleate by day 28. Endometrial granular cells became more conspicuous and appeared to increase in numbers adjacent to glands and blood vessels. Endometrial glands showed no notable changes, and were mostly tortuous with columnar epithelium and apocrine-type secretions. Around days 40 and 48 of the treatment cycle, the luminal margins of the glands became bosselated, and significant amounts of secretion were present in the glandular lumen. Measurement of immunoreactive concentrations of oestradiol-17β and progesterone in endometria from traumatized, hormone-treated monkeys revealed significant (P < 0·01) decreases in levels of oestradiol with time while the level of progesterone remained unchanged (P > 0·02). The corresponding profiles of concentrations of nuclear receptors for oestrogen and progesterone reflected the status of ligand availability in the endometrium; nuclear levels of progesterone receptors were maintained but significant decreases in cytoplasmic progesterone receptors (P < 0·03) and nuclear oestrogen receptors (P < 0·05) were evident with the period of treatment. Journal of Endocrinology (1989) 120, 51–58