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pubmed-article:3199799pubmed:abstractTextSpecific mouse monoclonal antibody (alpha PR6) against progesterone receptor was used with an avidin biotin complex technique to localize progesterone receptors in frozen sections of 26 normal cyclic human endometria. Progesterone receptor was detected in the nuclei of epithelial and stromal cells in both the functionalis and basalis layers. In the functionalis, the receptor content increased from the early to the late proliferative phase in both cell components. It remained high in the early secretory phase and decreased in the mid- and late secretory phases, comparatively more rapidly in the epithelium than in the stroma. In the latter, the predecidual cell nuclei were receptor-positive. The menstrual phase endometrium lacked receptors. The basalis was rich in progesterone receptors during the proliferative, early and midsecretory phases in both components and receptor-free during the late secretory and menstrual phases of the cycle. Myometrial smooth muscle cell nuclei contained progesterone receptors, whereas they were absent in endometrial and myometrial vessels. Overall, the epithelial progesterone receptor content seemed to correlate with the endometrial tissue levels of estradiol, possibly reflecting its estrogen sensitivity, whereas the stromal progesterone receptor content during the secretory phase at least, in part, may be constitutively synthetized.lld:pubmed
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pubmed-article:3199799pubmed:pagination862-9lld:pubmed
pubmed-article:3199799pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:3199799pubmed:year1988lld:pubmed
pubmed-article:3199799pubmed:articleTitleImmunocytochemical study of progesterone receptors in the human endometrium during the menstrual cycle.lld:pubmed
pubmed-article:3199799pubmed:affiliationDepartment of Pathology, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada.lld:pubmed
pubmed-article:3199799pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3199799pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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