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LH appears to be a potent stimulator of the release of endometrial prostaglandins (PGs) in the pig. The aim of the present studies was to examine the effect of LH on PGF_2α and PGE₂ secretion by cultured porcine endometrial cells on days 10–12 and 14–16 of the oestrous cycle and to compare its action with oxytocin. A time-dependent effect of LH (10 ng/ml) on PGF_2α release from luminal epithelial and stromal cells on days 10–12 was observed (experiment 1). The highest increase in PGF_2α secretion in response to LH was detected in stromal cells after 6 h of incubation (P < 0.001). Epithelial cells responded to LH after a longer exposure time (P < 0.01). A concentration-dependent effect of LH (0.1–100 ng/ml) on PGF_2α release from stromal cells was examined after 6 h and from epithelial cells after 12 h (experiment 2). Effective concentrations of LH were 10 and 100 ng/ml. LH (10 ng/ml) and oxytocin (100 nmol/l) affected PGF_2α and PGE₂ secretion from endometrial cells on days 10–12 and 14–16 of the oestrous cycle (experiment 3). LH stimulated PGF_2α secretion from both cell types and its action was more potent on days 10–12. LH induced PGE₂ release, especially in epithelial cells on days 14–16. A stimulatory effect of oxytocin on PGF_2α was confirmed in stromal cells, but this hormone was also shown to enhance PGE₂ output. These results indicated that LH, like oxytocin, a very effective stimulator of PGF_2α release, could play an important role in the induction of luteolysis.

Oxytocin (OXT) and tumor necrosis factor α (TNF) have been implicated in the control of luteolysis by stimulating endometrial secretion of luteolytic prostaglandin F_{2 α} (PGF_{2 α}). Nevertheless, OXT concentration in porcine uterine lumen increases markedly on days 11–12 of pregnancy, and TNF is expressed in endometrium during pregnancy. The objective of the study was to determine the effect of OXT and TNF on expression of the enzymes involved in PG synthesis: PG-endoperoxide synthase 2 (PTGS2), PGE₂ synthase (mPGES-1) and PGF synthase, and PGE₂ receptor (PTGER2), as well as on PG secretion by endometrial luminal epithelial cells (LECs) on days 11–12 of the estrous cycle and pregnancy. LECs isolated from gilts on days 11–12 of the estrous cycle (n=8) and pregnancy (n=7) were treated with OXT (100 nmol/l) and TNF (0.6 nmol/l) for 24 h. OXT increased PTGS2 mRNA and mPGES-1 protein contents, as well as PGE₂ secretion but only on days 11–12 of pregnancy. TNF stimulated PTGS2 and mPGES-1 mRNA, as well as mPGES-1 protein expression and PGE₂ release on days 11–12 of pregnancy and the estrous cycle. In addition, expressions of PTGER2 and PTGER4 were determined in corpus luteum (CL). Abundance of PTGER2 mRNA and PTGER4 protein in CL was upregulated on day 14 of pregnancy versus day 14 of the estrous cycle. This study indicates that TNF and OXT regulate PGE₂ synthesis in LECs during early pregnancy. PGE₂ secreted by LECs, after reaching ovaries, could have a luteoprotective effect through luteal PTGER2 and PTGER4, or may directly promote uterine function and conceptus development.

The new corpora lutea (CLs) in pigs are formed from the preovulatory follicles after the luteinizing hormone (LH) surge. However, total autonomy and independence of CLs from LH up to Day 12 of cycle has recently been questioned. Transformation of estrous cycle CL to CL of pregnancy initiated by embryonic signals requires not only the cessation of prostaglandin F2 (PGF_2α) supply to the luteal tissue but also needs the CL to overcome luteolytic acquisition and/or changing its sensitivity to PGF_2α during Days 12–14 of pregnancy. The luteolytic cascade is prevented by inhibition of lymphocyte infiltration and leucocyte recruitment, limitation of cell apoptosis, upregulation of pregnancy-associated genes and an enhanced antiluteolytic role of PGE₂. Our ‘two-signal switch hypothesis’ highlights the importance of post PGF_2α and PGE₂ receptor signaling pathways activation in CLs during luteolysis and rescue. The ‘luteolytic switch’ involves increased expression of many regression mediators and activation of the post PTGFR signaling pathway. The ‘rescue switch’ initiated by embryonic signals – estradiol 17β and PGE₂ – induces post PTGER2/4 pathway, turning the ‘luteolytic switch’ off and triggering activity of genes responsible for CL maintenance. In mid and late pregnancy, CLs are maintained by LH and the synergistic action of metabolic hormones. This paper provides an outline of recent views on CL regression, rescue and maintenance during pregnancy in pigs that conflict with previous paradigms and highlights new findings regarding the actions of prostaglandins, role of microRNAs (miRNA) and immune system and signaling pathways governing the life cycle of porcine CL.