Direct effects of the prostaglandins E2 and f2alpha on progesterone release by the corpus luteum of the marmoset monkey (Callithrix jacchus) studied by in vitro microdialysis

Abstract

The effects of the prostaglandins (PG) E 2 and F 2 on progesterone secretion in luteal tissue (32 corpora lutea) explanted from the mid-luteal ovary of the marmoset monkey (n=13) were investigated using an in vitro microdialysis system. Consecutive applications of 1, 10 and 100 µg/ml PGE 2 resulted in a significant increase in secretion of progesterone at the maximum dose of 100 µg/ml, which was shown to be the stimulatory dose in both long-period and 20-min pulse (time to collect one fraction) applications. The response varied individually between 1·4-and 3·4-fold above the baseline concentrations. Application of 500 µg/ml PGF 2 led to similar hormone responses. In contrast, lower doses of PGF 2 (0·5, 5 and 50 µg/ml) resulted in significantly increased levels of secretion of progesterone, to approximately 1·4-fold baseline values, only after the application was terminated (echo effect). Responses were less variable when a short pulse of 20 min duration was applied, instead of long applications of 1-2 h. On the basis of the passage rates measured for tritiated PGF 2 , transfer through the dialysis membrane was assumed to be in the range of 1% for both PGs. Ultrastructurally, luteal cells lying in a sheath of five to seven cell layers around the dialysis tubing appeared intact and were interconnected by gap junctions. Vesiculation of the smooth endoplasmic reticulum was more prominent after PG treatment, indicating a stimulation of cellular synthesis/secretory activities that was in accordance with the stimulatory action of both PGs on progesterone release under these in vitro conditions.

PTGER1 and PTGER2 receptors mediate regulation of progesterone synthesis and type 1 11β-hydroxysteroid dehydrogenase activity by prostaglandin E2 in human granulosa–lutein cells

“…The ability of PGE 2 to stimulate progesterone synthesis in human and non-human primate luteal cells, and in the widely used model of human granulosa–lutein cells, is well documented (Hahlin et al 1988, Fehrenbach et al 1999, Vaananen et al 2001). Given the reported ability of PGE 2 to increase intracellular cAMP concentrations in these cells (Michael et al 1993) and the established role for cAMP as a second messenger that stimulates steroidogenesis (Cooke 1999), it has widely been assumed that the progesterone response to PGE 2 is mediated via this cyclic nucleotide.…”