IMMUNOCYTOCHEMICAL COLOCALIZATION OF PROGESTERONE-RECEPTOR AND PROLACTIN IN INDIVIDUAL STROMAL CELLS OF HUMAN DECIDUA

Citation
Jd. Wang et al., IMMUNOCYTOCHEMICAL COLOCALIZATION OF PROGESTERONE-RECEPTOR AND PROLACTIN IN INDIVIDUAL STROMAL CELLS OF HUMAN DECIDUA, The Journal of clinical endocrinology and metabolism, 79(1), 1994, pp. 293-297
Citations number
24
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
79
Issue
1
Year of publication
1994
Pages
293 - 297
Database
ISI
SICI code
0021-972X(1994)79:1<293:ICOPAP>2.0.ZU;2-7
Abstract
Progesterone stimulates decidual PRL production. However, decidualized tissue, in which a high level of PRL is present, features a relativel y low level of progesterone receptor (PR) expression. The discrepancy has to be explored at the individual cell level. The present study emp loyed a double labeling method to colocalize PR and PRL in human decid ua to examine the correlation between these two proteins. In frozen se ctions, decidual stroma presented two kinds of cell, which differed in PRL staining. Decidualized cells were positively stained with PRL in cytoplasm and displayed a large cell size and a clear cell outline. No ndecidualized cells showed no specific PRL staining and no dear cell b oundary. In decidual stroma, PR staining was exclusively localized in the nuclei, with variations in intensity. When double staining with PR and PRL was performed, these two types of cells demonstrated diverse staining patterns. The PRL-producing cells exhibited weak PR staining, whereas PRL-negative cells evidenced stronger PR staining. In RU 486- treated samples, decidual stroma became less stained with PRL, compare d with the control, and fewer cells displayed typical morphology of de cidualization, whereas PR staining in the tissue became more extensive and intensive. Double labeling disclosed that the cells with enhanced PR staining were coupled to weaker PRL immunoreaction. Our data sugge sted an inverse relationship between PRL and PR in individual stromal cells in vivo, which could be reversed by antiprogestin treatment. A p ossible autocrine mechanism controlling this phenomenon was proposed a nd deserves further study.