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Androgens Upregulate Endometrial Epithelial Progesterone Receptor Expression: Potential Implications for
Samir N Babayev1, Chan Woo Park1,2, Patrick W Keller1
11 Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Reproductive Sciences (Thousand Oaks, Calif.)
|September 12, 2017
Summary
Androgens, like 5α-dihydrotestosterone (DHT), increase progesterone receptor (PR) expression in human endometrial cells. This androgenic effect on PR is mediated through the androgen receptor (AR), suggesting a novel mechanism for endometrial regulation.
Area of Science:
- Endocrinology
- Reproductive Biology
- Molecular Biology
Background:
- Androgenic compounds are linked to endometrial atrophy, but their mechanisms in the human endometrium are poorly understood.
- This study investigates if androgens influence endometrial function by modulating progesterone receptor (PR) expression.
Purpose of the Study:
- To determine the effect of 5α-dihydrotestosterone (DHT) on progesterone receptor (PR) expression in human endometrial cells.
- To elucidate the role of the androgen receptor (AR) in mediating androgenic effects on PR expression.
Main Methods:
- Human endometrial explants, stromal cells, and Ishikawa cells were treated with DHT.
- Androgen receptor (AR) blocker flutamide was used in combination with DHT in Ishikawa cells.
- PR isoforms (PR-A, PR-B), PR mRNA, and cell proliferation markers (cyclin D1, D2) were assessed.
Main Results:
- DHT increased PR expression in endometrial explants and Ishikawa cells, but not stromal cells.
- DHT elevated both PR-A and PR-B protein levels.
- Flutamide blocked DHT-induced PR upregulation, confirming AR mediation.
- DHT did not induce cell proliferation markers, unlike estradiol.
Conclusions:
- Androgens can upregulate PR gene and protein expression in the human endometrium.
- Androgen-mediated PR upregulation involves the androgen receptor (AR).
- This suggests a potential mechanism for androgen action in endometrial regulation.
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