Corpus luteum regression or maintenance: a duel between prostaglandins and interferon tau

Abstract

The corpus luteum (CL), via progesterone production, plays a central role in the regulation of cyclicity and in the establishment and maintenance of pregnancy in ruminant species. In the absence of an embryonic signal, the CL will regress functionally and then structurally. Pulses of prostaglandin F2α (PGF2α) from the uterus reach the ovary via the vascular utero-ovarian plexus causing the demise of the CL. Although it is well established that PGF2α is the principal luteolytic hormone in ruminants, many aspects of its function are still being debated. The successful establishment of pregnancy requires inhibition of uterine PGF2α actions, prolongation, or maintenance of luteal function and the continuous secretion of progesterone. The conceptus signals its presence by releasing interferon tau (IFNT). IFNT acting directly on the endometrium by various mechanisms and possibly also on the CL activates antiluteolytic responses that protect the function of the CL. PGE2, synthesized by the endometrium and the CL, could also induce processes that are important for maintenance of luteal function in pregnancy. The mechanisms controlling luteal regression or its maintenance by the coordinated actions of PGF2α, IFNT, and PGE2 are discussed.