Review: Luteal prostaglandins: mechanisms regulating luteal survival and demise in ruminants

The corpus luteum (CL) is critical for establishment and maintenance of pregnancy in all mammals. However, the fate of the CL in ruminants is dependent on the presence of a functional uterus or signals from a developing embryo to modify uterine function to ensure its own survival. The key molecule secreted by the uterus that must be modified is prostaglandin F2alpha (PGF2A). At the same time, there is evidence that mechanisms within the CL may influence the ability of PGF2A to cause luteolysis. This review focuses on prostaglandins and steroidogenic capacity as endogenous modulators of the sensitivity of the CL to exogenous PGF2A. Early luteal development and early pregnancy are two different luteal stages in which sensitivity of the CL to PGF2A renders it incapable, or less capable, respectively, of undergoing luteolysis in response to PGF2A compared to a midcycle CL. An analysis of molecular changes that occur during these two stages provides some novel insight into molecules and pathways worth exploring to explain the regulation of luteolytic capacity in corpora lutea of ruminants.