Luteal regression is caused by a pulsatile release of prostaglandin (PG) F2α from the uterus in the late luteal phase in most mammals including cattle. Although it has been proposed in ruminants that pulsatile PGF2α secretion is generated by a positive feedback loop between luteal and/or hypophyseal oxytocin and uterine PGF2α, the bovine endometrium may possess other mechanisms for initiation of luteolytic PGF2α secretion. It has been recently demonstrated that tumor necrosis factor-α (TNF-α) stimulates PGF2α output from bovine endometrial tissue not only during the follicular phase but also during the late luteal phase, suggesting that TNF-α is a factor in the initiation of luteolysis in cattle. Furthermore, our recent study has shown that IFN-τ suppresses the action of TNF-α on PGF2α synthesis by the bovine endometrium in vitro, suggesting that IFN-τ plays a luteoprotective role by inhibiting TNF-α-induced PGF2α production in early pregnancy. On the other hand, factors other than oxytocin or TNF-α have also been suggested to be involved in the regulation of PGF2α synthesis by bovine endometrium. The purpose of this review is to summarize our current understanding of the endocrine mechanisms that regulate the timing and pattern of uterine PGF2α secretion during the estrous cycle and early pregnancy.
ASJC Scopus subject areas
- Animal Science and Zoology