Immunocytochemical colocalization of progesterone receptor and prolactin in individual stromal cells of human decidua

• Published in: The journal of clinical endocrinology and metabolism Vol. 79; no. 1; p. 293
• Main Authors: Wang, J D, Zhu, J B, Shi, W L, Zhu, P D
• Format: Journal Article
• Language: English
• Published: United States 01.07.1994
• Subjects: Cell Nucleus - chemistry; Cytoplasm - chemistry; Decidua - chemistry; Decidua - drug effects; Decidua - ultrastructure; Female; Humans; Immunohistochemistry; Mifepristone - pharmacology; Pregnancy; Prolactin - analysis; Receptors, Progesterone - analysis; Tissue Distribution
• ISSN: 0021-972X
• DOI: 10.1210/jc.79.1.293

Progesterone stimulates decidual PRL production. However, decidualized tissue, in which a high level of PRL is present, features a relatively low level of progesterone receptor (PR) expression. The discrepancy has to be explored at the individual cell level. The present study employed a double labeling method to colocalize PR and PRL in human decidua to examine the correlation between these two proteins. In frozen sections, 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. Nondecidualized cells showed no specific PRL staining and no clear cell boundary. 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, compared with the control, and fewer cells displayed typical morphology of decidualization, 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 suggested an inverse relationship between PRL and PR in individual stromal cells in vivo, which could be reversed by antiprogestin treatment. A possible autocrine mechanism controlling this phenomenon was proposed and deserves further study.