Abstract
Abstract
During menses in the primate, zone I and parts of zone II of the endometrium are sloughed, and subsequently reconstruction of the endometrium for the next cycle begins. In this study we examined the cell type and zonal changes in estrogen (E) and progesterone (P) receptors (R) that occur during these changes in endometrial structure and the coincident changes in hormonal stimulation. Immunohistochemical analyses of ERα and PR were performed on endometrial biopsies obtained during artificial menstrual cycles in the rhesus monkey on day 26 (declining serum P), Days 1 and 3 of menses, and Day 5 (following endometrial reconstruction). The pattern and distribution of ERα and PR in the endometrium on Day 26 was similar to that observed previously on Day 23; ERα and PR showed strong positive staining for glandular epithelia in zone IV of the basalis and little or no staining for ERα in zones I and II-III whereas PR showed positive staining in stromal cells and little or no staining in epithelia in zones I and II-III. On Day 1 of menses, no detectable ERα and PR staining was observed in glandular epithelial throughout the endometrium. PR immunoreactivity remained in stromal cells on Day 1 whereas ERα staining returned to stromal cells reflecting a release from P inhibition of ERα. By Day 3 of menses positive staining for ERα and PR was observed in glandular epithelia in zones II-III and zone IV. By Day 5 the reconstruction of the endometrium was complete, and strong positive staining for both receptors was present throughout the endometrium. Following removal of all E stimulation on Day 26, no distinct differences in receptor distribution were observed on Day 3. These data suggest that hormone-independent mechanisms such as in normal wound healing are also operative during menses and reconstruction. The presence of ERα, primarily in stromal cells during normal menses, supports the notion that the mesenchymal compartment plays an important role in the orchestration of normal endometrial reconstruction in response to E.
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