Estradiol-17&amp;#946; altera expressão proteica endometrial em fêmeas bovinas tratadas no 17º dia do ciclo estral

Alves, Sérgio Silva; Castro, Fernanda Cavallari de; Soares, Natalia Costa; Pereira, Flávia Thomaz Veréchia; Balieiro, Júlio César de Carvalho; Munin, Flávia Simone; Cesar, Marcelo de Cerqueira; Binelli, Mário; Membrive, Claudia Maria Bertan

doi:10.11606/s1413-95962011000100004

Cited by 1 publication

(2 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In Oliveira (2017), the hypothesis that 17β-E 2 would stimulate was also rejected, which corroborates with our results (in Experiments 1 and 2). Alves et al (2011) demonstrated that in vivo treatment with 17β-E 2 did not modulate the total protein amount in endometrial explants collected 2 h after slaughter. There was also no modulation in the abundance of proteins with molecular weights similar to PKC (approximately 80 kDa).…”

Section: Discussionmentioning

confidence: 92%

“…There was also no modulation in the abundance of proteins with molecular weights similar to PKC (approximately 80 kDa). However, Alves et al (2011) reported an increase in the number of proteins with molecular weights of 75 to 76 kDa and 108 to 110 kDa. Thus, it is suggested that other proteins, which we did not evaluate, may modulate PGF2α synthesis by stimulating 17β-E 2 .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Use of protein kinase C and phospholipase A2 inhibitors in bovine endometrial cells treated with estradiol and calcium ionophore

Maldonado

Ciriaco

Ferreira

et al. 2021

Braz. J. Vet. Res. Anim. Sci.

Self Cite

View full text Add to dashboard Cite

The release of endometrial prostaglandin-F2α (PGF2α) in bovine females can be induced in vivo by estradiol (E2). However, its role in this mechanism has not been clarified. We hypothesized that E2 stimulates the activity and abundance of protein kinase C (PKC) and phospholipase A2 (PLA2). Our objective in this study was to analyze the effects of PKC and PLA2 inhibitors on PGF2α synthesis induced by E2 and calcium ionophore (CI) in bovine endometrial cells (BEND cells; Experiment 1). Additionally, we evaluated the abundance of PKC and PLA2 in endometrial explants of cows treated or not with E2 17 days after estrus (D17, D0 = estrus; Experiment 2). In Experiment 1, BEND cells were submitted to a PKC inhibitor (10 μM of C25H24N4O2; bisindolylmaleimide I, or BIS I), a PLA2 inhibitor (20 μM of arachydoniltrifluoromethane or AACOCF3), or none. The BEND cells were subsequently treated with E2 and CI, and PGF2α concentrations were measured in the culture medium through radioimmunoassay. For DIF-12 (PGF2α concentration 12 h after treatment subtracted from PGF2α concentration at hour 0), no PKC inhibitor effect was observed (P= 0.2709). However, DIF-12 was lower (P < 0.05) for groups treated with the PLA2 inhibitor and PLA2 inhibitor + CI + E2 groups than the control and CI + E2 groups. Thus, AACOCF3 was an efficient PLA2 inhibitor in the BEND cells culture system, and E2 did not stimulate the synthesis of PKC and PLA2. In Experiment 2, cyclic Nellore heifers received none (n = 5) or 3 mg (n = 6) of 17β-E2 on D17 and were slaughtered 2 h after administration. The abundance of PKC and PLA2 in the endometrial tissue was evaluated using Western blotting analysis. No E2 effect was observed on PKC (P = 0.08) and PLA2 (P = 0.56). We concluded that E2 did not stimulate the activity and abundance of PKC and PLA2.

show abstract

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%