Prostaglandins produced within the CL may serve as local modulators of CL function. The present study was designed to characterize the cellular mechanisms by which the cytokine interleukin-1β (IL-1β) stimulates prostaglandin production in cultured luteal cells. Cycloheximide (CHX) and actinomycin D (Act D) did not affect basal, but completely inhibited IL-1β- stimulated prostaglandin F(2α) (PGF(2α)) production (p < 0.05). The phospholipase A2 (PLA2) inhibitor, aristolochic acid (PLA2X), and the phospholipase C (PLC) inhibitor, compound 48/80 (PLCX), suppressed IL-1β- stimulated (p < 0.05), but not basal, PGF(2α) production. The addition of exogenous arachidonic acid (AA) restored the stimulatory effect of IL-1β in PLCX-treated, but not in PLA2X-treated, cells, suggesting that PLA2 is a key regulatory point of IL-1β action. Chronic exposure of the luteal cells to IL-1β resulted in stimulatory effects beyond that of increasing AA availability, presumably by up-regulation of prostaglandin endoperoxide (PGH) synthase. Chronic exposure of luteal cells to IL-1β also inhibited progesterone production, but this effect appeared to be independent of endogenous PGF(2α) production. The ability of IL-1β to comprehensively stimulate luteal PGF(2α) production while inhibiting luteal progesterone production is suggestive that IL-1β may facilitate regression of the CL.
All Science Journal Classification (ASJC) codes
- Reproductive Medicine
- Cell Biology