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  • Title: A zonal pattern of cell proliferation and differentiation in the rhesus endometrium during the estrogen surge.
    Author: Padykula HA, Coles LG, McCracken JA, King NW, Longcope C, Kaiserman-Abramof IR.
    Journal: Biol Reprod; 1984 Dec; 31(5):1103-18. PubMed ID: 6518227.
    Abstract:
    The cellular and tissue basis of endometrial renewal in the rhesus monkey is being investigated by radioautographic localization of proliferating cell populations. Here we report our findings on epithelial cell proliferation during the midcycle estrogen surge. Endometrial biopsies were obtained by hysterotomy at approximately 1 h after a single intravascular injection of [3H] thymidine ([3H]T). Light and electron microscopic radioautography was performed on 7 specimens obtained from 4 monkeys in relation to the serum estradiol (E2) peak as follows: -2, -1, 0, +1, +2, and +3 days (+/- 1 day). Cell proliferation and differentiation were analyzed according to the 4 horizontal histologic endometrial zones (Bartelmez et al., 1951). Epithelial labeling indices were higher in the functionalis (Zone I, luminal epithelium, 9-12%; Zone II, uppermost gland segments, 7-14%) than in the basalis (Zone III, middle gland segments, 5-7%; and Zone IV, basal gland segments, 1-7%). Despite the large and rapid serum E2 fluctuations during the surge from -2 days to +3 days E2 peak, proliferating epithelial populations within Zones I, II and III remained quite uniform in size. In the basalis, the proliferative patterns of Zones III and IV were dissimilar. The labeling index of Zone III remained quite uniform (5-7%), whereas in Zone IV, it increased progressively from 1% (-2 days) to 7% (+3 days). These data establish the bipartite nature of the basalis. Radioautographic evidence indicates that endometrial cell proliferation is tightly coupled to progressive cell differentiation in the functionalis and basalis. Thus intrinsic positional differences exist in the responsiveness of the primate endometrium to common hormonal stimulation during the E2 surge and the initial postovulatory rise of progesterone.
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