Oliveira, M. L.
Mello, B. P.
Gonella-Diaza, A. M.
Scolari, S. C.
Feltrin, I. R.
Canavessi, A. M. O.
Membrive, C. M. B.
Total Authors: 11
 State Univ Maranhao Tocantine Reg, Agr Sci Ctr, 1300 Godofredo Viana St, BR-65900000 Imperatriz, MA - Brazil
 Univ Sao Paulo, Dept Anim Reprod, 225 Duque de Caxias Norte Ave, BR-13635900 Pirassununga, SP - Brazil
 Univ Florida, North Florida Res & Educ Ctr, Inst Food & Agr Sci, 3925 FL-71, Greenwood, FL 32443 - USA
 Sao Paulo State Univ, Dept Pharmacol & Biotechnol, BR-18618970 Botucatu, SP - Brazil
 Univ Sao Paulo, Luiz de Queiroz Coll Agr, Dept Anim Sci, 11 Padua Dias Ave, BR-13418900 Piracicaba, SP - Brazil
 Sao Paulo State Univ, Dept Anim Sci, 294 SP Commander Joao Ribeiro de Barros, 651 Rd, BR-17900000 Dracena, SP - Brazil
Total Affiliations: 7
DOMESTIC ANIMAL ENDOCRINOLOGY;
Web of Science Citations:
In cattle, 17 beta-estradiol (E2) stimulates prostaglandin F2 alpha (PGF2 alpha) synthesis, which causes luteolysis. Except for the well-established upregulation of oxytocin receptor gene (OXTR), molecular mechanisms of E2-induced PGF2 alpha release in vivo remain unknown. We hypothesized that E2-induced PGF2 alpha release requires de novo transcription of components of the PGF2 alpha synthesis machinery. Beef cows (n = 52) were assigned to remain untreated (Con-trol; n = 10), to receive 50% ethanol infusion intravenously (Placebo; n = 21), or 3 mg E2 in 50% ethanol infusion intravenously (Estradiol; n = 21) on day 15 (D15) after estrus. We collected a single endometrial biopsy per animal at the time of the treatment (0h; Control B0h group), 4 hours (4h; Placebo B4h group and Estradiol B4h group), or 7 hours (7h; Placebo B7h group and Estradiol B7h group) post-treatment. Compared to the Placebo group, the Estradiol group presented significantly greater 13,14-dihydro-15-keto-PGF2 alpha con-centrations between 4h and 7h and underwent earlier luteolysis. At 4h, the qPCR analysis showed a lower abundance of ESR1, ESR2 and aldo-keto reductase family 1 member B1 (AKR1B1) genes in the Estradiol B4h group, and a greater abundance of OXTR compared to the Placebo B4h group. Similarly, the E2 treatment significantly reduced the abundance of AKR1B1, and AKR1C4 in the Estradiol B7h group, compared to the placebo group. Overall, E2-induced PGF2 alpha release and luteolysis involved an unexpected and transient downregulation of components of the PGF2 alpha-synthesis cascade, except for OXTR, which was up-regulated. Collectively, our data suggest that E2 connects newly-synthesized OXTR to pre-existing cellular machinery to synthesize PGF2 alpha and cause luteal regression. (C) 2021 Elsevier Inc. All rights reserved. (AU)