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Dependence on Prolactin of the Luteolytic Effect of Prostaglandin F₂ in Rat Luteal Cell Cultures¹

^a Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa 31096, Israel

ABSTRACT

Luteal regression is a multistep, prolonged process, and long-term luteal cultures are required for studying it in vitro. Cell suspensions from ovaries of superovulated rats were enriched with steroidogenic cells, seeded on laminin or fibronectin, and maintained in defined medium for up to 10 days. Progesterone secretion was much lower than that of 20-dihydroprogesterone, a product of 20-hydroxysteroid dehydrogenase (20-HSD). Prolactin added throughout the incubation period gradually increased the percent progesterone out of total progestins to fourfold, while reducing 20-HSD mRNA by 73%. Luteinizing hormone accelerated the establishment of higher percent progesterone by prolactin but by itself had no effect. Prolactin did not increase total progestin production or cytochrome P450 side-chain cleavage (P450_scc) mRNA. Cell viability was unaffected by prolactin and/or LH. Prostaglandin F₂ (PGF₂) was added 7–8 days after seeding. In prolactin-treated cells, PGF₂ reduced steroidogenesis after 4–45 h, and at 45 h total progestins and P450_scc mRNA were reduced by 45%. At 8–45 h PGF₂ reduced the percent progesterone out of total progestins, and at 45 h 20-HSD mRNA was doubled. In contrast, in prolactin-deprived cultures, PGF₂ had little effect on total progestins or 20-HSD mRNA but doubled P450_scc mRNA. Phospholipase C activity was stimulated by PGF₂ regardless of prolactin. Thus, when prolactin-treated, our cultures are a good model for mature corpora lutea challenged with PGF₂; the finding that without prolactin PGF₂ has an alternative set of actions could help in identifying the signaling pathways of PGF₂ responsible for its luteolytic effects.

FOOTNOTES

First decision: 6 March 2001.

¹ Supported in part by the Chief Scientist of the Israel Ministry of Health, the Dario and Mathilde Beraha Fund for Hormones and Aging Research, and the Technion Vice President of Research Fund, Hedson Fund for Medical Research.

² Correspondence: Michal Lahav, Unit of Endocrinology, Room 5-25, Bruce Rappaport Faculty of Medicine, The Technion, P.O. Box 9649, Efron Street, Bat Galim, Haifa 31096, Israel. FAX: 972 4 8532102; mlahav{at}tx.technion.ac.il

³ These authors contributed equally to the present study.

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				C. Stocco, C. Telleria, and G. Gibori The Molecular Control of Corpus Luteum Formation, Function, and Regression Endocr. Rev., February 1, 2007; 28(1): 117 - 149. [Abstract] [Full Text] [PDF]