Activation of elements of the phosphatidylinositol pathway in the primate corpus luteum by prostaglandin E2.

The current study was designed to examine the effects of prostaglandin (PG) E2 on progesterone production by primate luteal cells collected during the late luteal phase. PGE2 inhibited basal and human chorionic gonadotrophin (HCG)-stimulated progesterone production (P < 0.01) in late luteal phase corpora lutea. The ability of PGE2 to activate a second messenger system (phosphatidylinositol pathway) in corpora lutea of rhesus monkeys was also assessed. PGE2 significantly increased the accumulation of inositol phosphates (P < 0.05). This stimulation was not apparent in the early luteal phase but was manifested in the mid-late luteal phase. PGE2 also caused a rapid, yet transient, increase (P < 0.01) in intracellular free calcium ion concentrations ([Ca2+]i) in a large proportion of primate luteal cells. The proportion of luteal cells that responded to PGE2 with an increase in [Ca2+]i was smaller (P < 0.05) in corpora lutea collected during the early luteal phase (12%) in comparison with those collected during the latter half of the luteal phase (63-66%). Changes in [Ca2+]i in response to PGE2 were similar in small and large luteal cells. This study demonstrates that PGE2 activates elements of the phosphatidylinositol pathway in primate corpora lutea. This activation is augmented as the luteal phase progresses. Thus, the inhibitory effects of PGE2 on luteal progesterone production observed in the late luteal phase are associated with activation of elements of the phosphatidylinositol pathway.