The role of PGE2 and PGF2a in follicle wall rupture and their implications in the development and treatment of luteinized unruptured follicles

The role of PGE2 and PGF2a in follicle wall rupture and their implications in the development and treatment of luteinized unruptured follicles

Die Rolle von PGE2 and PGF2α bei der Ruptur der Follikelwand und ihre Auswirkungen auf die Entwicklung und Behandlung luteinisierter nicht-rupturierter Follikel

Cuervo-Arango J, Martínez-Boví R

DOI: 10.21836/PEM20160110
Year: 2016
Volume: 32
Issue: 1
Pages: 54-56

This manuscript summarizes the results of several studies, which highlight the relevance of prostaglandins E2 (PGE2) and F2α (PGF2α) during the ovulatory process in mares and their implication in the pathogenesis of luteinized unruptured follicles. Following the preovulatory luteinizing hormone (LH) surge, the two prostaglandins are synthesized in granulosa cells. They subsequently trigger a cascade of events that lead to ovulation. The exogenous administration of intrafollicular PGE2 and PGF2α can induce follicle rupture and ovulation within 12 h of injection, even in mares in early estrus, and before the beginning of the abrupt rise of the preovulatory LH surge. The systemic administration of a prostaglandin synthesis inhibitor (flunixin-meglumine) during the periovulatory period blocks ovulation and induces the development of luteinized unruptured follicles (LUFs). LUFs share similar ultrasonographic and hormonal characteristics with hemorragic anovulatory follicles (HAFs). The administration of intrafollicular PGE2 and PGF2α in mares treated with a prostaglandin synthesis inhibitor restores normal ovulation and allows oocyte release and fertilization. However, the systemic administration of prostaglandins does not appear to have any effect on hastening ovulation.