Unravelling the role of 17β-estradiol on advancing uterine luteolytic cascade in cattle

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dc.contributor.authorOliveira, M. L.
dc.contributor.authorMello, B. P.
dc.contributor.authorGonella-Diaza, A. M.
dc.contributor.authorScolari, S. C.
dc.contributor.authorPugliesi, G.
dc.contributor.authorMartins, T.
dc.contributor.authorFeltrin, I. R. [UNESP]
dc.contributor.authorSartori, R.
dc.contributor.authorCanavessi, A. M.O.
dc.contributor.authorBinelli, M.
dc.contributor.authorMembrive, C. M.B. [UNESP]
dc.contributor.institutionState University of Maranhão Tocantine Region
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversity of Florida
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.date.accessioned2022-04-28T19:43:42Z
dc.date.available2022-04-28T19:43:42Z
dc.date.issued2022-01-01
dc.description.abstractIn cattle, 17β-estradiol (E2) stimulates prostaglandin F2α (PGF2α) synthesis, which causes luteolysis. Except for the well-established upregulation of oxytocin receptor gene (OXTR), molecular mechanisms of E2-induced PGF2α release in vivo remain unknown. We hypothesized that E2-induced PGF2α release requires de novo transcription of components of the PGF2α synthesis machinery. Beef cows (n = 52) were assigned to remain untreated (Control; 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-PGF2α concentrations 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 PGF2α release and luteolysis involved an unexpected and transient downregulation of components of the PGF2α-synthesis cascade, except for OXTR, which was upregulated. Collectively, our data suggest that E2 connects newly-synthesized OXTR to pre-existing cellular machinery to synthesize PGF2α and cause luteal regression.en
dc.description.affiliationAgrarian Sciences Center State University of Maranhão Tocantine Region
dc.description.affiliationDepartment of Animal Reproduction University of São Paulo
dc.description.affiliationNorth Florida Research and Education Center Institute of Food and Agricultural Sciences University of Florida
dc.description.affiliationDepartment of Animal Sciences University of Florida
dc.description.affiliationDepartment of Pharmacology and Biotechnology São Paulo State University
dc.description.affiliationDepartment of Animal Science Luiz de Queiroz College of Agriculture University of São Paulo
dc.description.affiliationDepartment of Animal Sciences São Paulo State University
dc.description.affiliationUnespDepartment of Pharmacology and Biotechnology São Paulo State University
dc.description.affiliationUnespDepartment of Animal Sciences São Paulo State University
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFAPESP: 2015/03331-3)
dc.identifierhttp://dx.doi.org/10.1016/j.domaniend.2021.106653
dc.identifier.citationDomestic Animal Endocrinology, v. 78.
dc.identifier.doi10.1016/j.domaniend.2021.106653
dc.identifier.issn0739-7240
dc.identifier.scopus2-s2.0-85113497255
dc.identifier.urihttp://hdl.handle.net/11449/222281
dc.language.isoeng
dc.relation.ispartofDomestic Animal Endocrinology
dc.sourceScopus
dc.subjectEndometrium
dc.subjectEstrogen
dc.subjectLuteolysis
dc.subjectProstaglandin
dc.titleUnravelling the role of 17β-estradiol on advancing uterine luteolytic cascade in cattleen
dc.typeArtigo

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