Elevated prostaglandin F2 alpha after the period of embryonic secretion of interferon tau appears to be due to upregulation of uterine synthesis machinery for prostaglandin F2 alpha.

During early pregnancy, the embryo interacts with the maternal system to prevent uterine secretion of prostaglandin F2 alpha (PGF2α) to allow for luteal maintenance. After day 25 basal PGF2α is upregulated; however, it does not cause luteolysis. We determined the uterine cervical and luteal transcriptomic profile associated with greater secretion of PGF2α on days 30 (P30) and 50 (P50) of gestation in contrast with day 15 of the estrous cycle in nonpregnant (non-bred) cows (NP15). Concentrations of PGF2α metabolite were greatest in P50, intermediate in P30, and least in NP15 (48.4 ± 3.9, 29.9 ± 2.6, and 9.6 ± 2.1 pg/mL, respectively). Cervical abundance of estradiol receptor 1 (ESR1), progesterone receptor, oxytocin receptor, and PGF2α synthase (AKRIB1) were greater in P50 compared to NP15. The ESR1 in P30 was greater than NP15 but less than P50. Estradiol receptor 2, an ESR1 inhibitor, was greater in NP15 than P30 and P50 and tended to be less in P50 compared to P30. Luteal prostaglandin transporter was greater in P30 and P50 compared to NP15 and aldo-keto reductase family 1 member C4 was greater in P50 compared to NP15. Luteal expression of PGF2α receptor was greater in P50 and P30 (tendency) compared to NP15. Luteal oxytocin/neurophysin 1 was greatest in NP15, intermediate in P30, and lowest in P50. Lastly, luteal hydroxyprostaglandin dehydrogenase 15-(NAD) is greater in P50 than in NP15. The current data suggests that the elevated PGF2α production during pregnancy appears to be due to upregulation of the uterine synthesis machinery for PGF2α. Luteal synthesis of PGF2α during pregnancy is not evident.