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Coordinated Regulation Among Progesterone, Prostaglandins, and EGF-Like Factors in Human Ovulatory Follicles

Artikel i vetenskaplig tidskrift
Författare Y. Choi
K. Wilson
P. R. Hannon
K. L. Rosewell
Mats Brännström
J. W. Akin
T. E. Curry
M. Jo
Publicerad i Journal of Clinical Endocrinology & Metabolism
Volym 102
Nummer/häfte 6
Sidor 1971-1982
ISSN 0021-972X
Publiceringsår 2017
Publicerad vid Institutionen för kliniska vetenskaper, sektionen för kvinnors och barns hälsa, Avdelningen för obstetrik och gynekologi
Sidor 1971-1982
Språk English
Länkar https://doi.org/10.1210/jc.2016-315...
Ämnesord bovine preovulatory follicles, human chorionic-gonadotropin, messenger-ribonucleic-acid, human granulosa-cells, endoperoxide, synthase-2, periovulatory interval, growth-factors, receptor, expression, inhibition, Endocrinology & Metabolism
Ämneskategorier Endokrinologi och diabetes

Sammanfattning

Context: In animal models, the luteinizing hormone surge increases progesterone (P4) and progesterone receptor (PGR), prostaglandins (PTGs), and epidermal growth factor (EGF)-like factors that play essential roles in ovulation. However, little is known about the expression, regulation, and function of these key ovulatory mediators in humans. Objective: To determine when and how these key ovulatory mediators are induced after the luteinizing hormone surge in human ovaries. Design and Participants: Timed periovulatory follicles were obtained from cycling women. Granulosa/lutein cells were collected from in vitro fertilization patients. Main Outcome Measures: The in vivo and in vitro expression of PGR, PTG synthases and transporters, and EGF-like factors were examined at the level of messenger RNA and protein. PGR binding to specific genes was assessed. P4 and PTGs in conditioned media were measured. Results: PGR, PTGS2, and AREG expressions dramatically increased in ovulatory follicles at 12 to 18 hours after human chorionic gonadotropin (hCG). In human granulosa/lutein cell cultures, hCG increased P4 and PTG production and the expression of PGR, specific PTG synthases and transporters, and EGF-like factors, mimicking in vivo expression patterns. Inhibitors for P4/PGR and EGF-signaling pathways reduced hCG-induced increases in PTG production and the expression of EGF-like factors. PGR bound to the PTGS2, PTGES, and SLCO2A1 genes. Conclusions: This report demonstrated the time-dependent induction of PGR, AREG, and PTGS2 in human periovulatory follicles. In vitro studies indicated that collaborative actions of P4/PGR and EGF signaling are required for hCG-induced increases in PTG production and potentiation of EGF signaling in human periovulatory granulosa cells.

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