Progesterone production by dispersed luteal cells obtained from the marmoset monkey on day 14 after ovulation can be stimulated by both prostaglandin F2α (PGF2α) 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, PGF2α 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 PGF2α 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 PGF2α/cloprostenol respectively. Hence, we conclude that the luteotrophic actions of prostaglandins E2 and F2α 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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