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Prolactin and its receptor in human endometrium
1Department of Obstetrics, Gynecology and Reproductive Medicine, State University of New York at Stony Brook 11794, USA.
Seminars in Reproductive Endocrinology
|July 16, 1999
Summary
Progestin and relaxin stimulate endometrial prolactin (PRL) and its receptor (PRL-R) production, crucial for pregnancy. Antiprogestin RU 486 initially boosts PRL but inhibits PRL-R, impacting fertility.
Area of Science:
- Reproductive Biology
- Endocrinology
- Molecular Genetics
Background:
- Prolactin (PRL) and its receptor (PRL-R) are synthesized in the human endometrium during the luteal phase and pregnancy.
- Hormonal regulation of endometrial PRL and PRL-R is critical for reproductive success.
Purpose of the Study:
- To investigate the hormonal requirements for sustained PRL and PRL-R production in long-term primary endometrial cell cultures.
- To elucidate the role of progestin, antiprogestin RU 486, and relaxin (RLX) in regulating endometrial PRL synthesis and PRL-R expression.
Main Methods:
- Long-term primary cell culture of human endometrial stromal cells.
- Hormonal treatments with progestin, RU 486, and RLX.
- Analysis of PRL and PRL-R mRNA levels and PRL production rates.
Main Results:
- Progestin induces PRL and PRL-R production during decidualization, increasing PRL gene transcription.
- RU 486 causes transient PRL superinduction but inhibits PRL-R mRNA expression.
- Relaxin enhances PRL synthesis, while PRL exhibits dual concentration-dependent effects on endometrial cell growth.
Conclusions:
- Endometrial PRL and PRL-R synthesis are tightly regulated by hormones like progestin and RLX.
- PRL and PRL-R play vital roles in implantation and pregnancy maintenance, with autocrine signaling influencing endometrial function.
- Decidual-derived prolactin is essential for regulating fetal fluid and electrolyte balance during gestation.