Up-regulation of the human prolactin receptor in the endometrium.

In humans, uterine endometrial stromal cells differentiate (decidualize) into decidual cells that express prolactin (PRL). Decidual PRL expression continues throughout pregnancy, thus decidual cells lining fetal membranes of term placenta synthesize and secrete PRL. To examine the hypothesis that PRL may play an autocrine role in the decidual cells, we examined the expression of the PRL receptor (PRL-R) during in vitro decidualization of stromal cells and in term decidua. In endometrial stromal cells decidualized by treatment with 1 μM medroxyprogesterone and 10 nM estradiol for 3, 6, and 9 d, respectively, a 12.7 kb PRL-R transcript increased 3-3.5-fold, 16.5-17-fold, and 23.5-24-fold, respectively, compared with untreated controls, in duplicate experiments. Progesterone-dependent PRL-R and PRL expression were stimulated by 1 μ/M prostaglandin E(2). Term decidua expressed the long form of the PRL-R and five major PRL-R transcripts (12.7, 9.7, 7.0, 3.6, and 2.8 kb). In contrast, human liver expressed two major transcripts (12.7 and 9.7 kb) while hepG2 cells expressed a single 7.0-kb-sized transcript. These studies demonstrate that PRL-R expression is stimulated upon progesterone-induced PRL gene expression in endometrial stromal cells supporting the hypothesis that PRL may have an autocrine effect in the endometrium and decidua.