“…Parturition in the ewe is initiated by activation of the fetal hypothalamic-pituitary-adrenal axis, followed by a concurrent increase in plasma cortisol and oestradiol production, that up-regulates PTGS2 expression and down-regulates PG dehydrogenase (PGDH), resulting in increased PG synthesis [20]. In the late pregnant ewe, PGE2 is produced primarily by the fetal component of the placentome, and concentrations rise over the last 3 weeks of gestation to aid fetal maturation [21]. At term, PGE2 causes cervical dilatation whereas PGF2α is released through oxytocin (OT) binding to its receptors in the intercotyledonary endometrium and stimulates uterine contractions and delivery [20,22,23].…”