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Progesterone production by dispersed luteal cells obtained from the marmoset monkey on day 14 after ovulation can be stimulated by both prostaglandin F₂ (PGF₂) and its structural analogue, cloprostenol. To establish whether these responses can be attributed to cross-reaction with the prostaglandin E₂ (PGE₂) receptor, this study compared the involvement of cyclic adenosine-3',5'-monophosphate (cAMP) and protein kinase C (PKC) in the luteotrophic responses to PGE₂, PGF₂ and cloprostenol. While all three prostaglandins stimulated similar increases in progesterone production (239·5 ± 7·9% of control; P <0·01), only PGE₂ stimulated a significant increase in cAMP accumulation (373·2 ± 28·4% of control; P <0·01). This study is the first to demonstrate PKC activity in the marmoset ovary. Following down-regulation of PKC with a tumour-promoting phorbol ester, 4β-phorbol 12-myristate 13-acetate (4β-PMA), basal progesterone production was significantly increased (150·9 ± 8·2% of control; P <0·05) and the luteotrophic effects of PGF₂ and cloprostenol were no longer evident, whereas the response to PGE₂ was unaffected. These observations are consistent with the differential involvement of cAMP and PKC in the luteotrophic responses to PGE₂ and PGF₂/cloprostenol respectively. Hence, we conclude that the luteotrophic actions of prostaglandins E₂ and F₂ on dispersed marmoset luteal cells are mediated via different receptors and signal transduction pathways.

Journal of Endocrinology (1993) 138, 291–298

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