Cynthia B.,CONICET |
Cynthia B.,Laboratorio Of Biologia Of La Reproduccion Labir |
Cristina D.B.,Laboratorio Of Biologia Of La Reproduccion Labir |
Adriana V.O.,CONICET |
And 5 more authors.
Journal of Steroid Biochemistry and Molecular Biology | Year: 2013
The aims of this work were to investigate if oestradiol 10-8 M in the incubation media of either the ovary alone (OV) or the ganglion compartment of an ex vivo coeliac ganglion-superior ovarian nerve-ovary system (a) modifies the release of ovarian progesterone (P4) and oestradiol (E2) on dioestrus II, and (b) modifies the ovarian gene expression of 3β-HSD and 20α-HSD enzymes and markers of apoptosis. The concentration of ovarian P4 release was measured in both experimental schemes, and ovarian P4 and E2 in the ex vivo system by RIA at different times. The expression of 3β-hydroxysteroid dehydrogenase, 20α-hydroxysteroid dehydrogenase and antiapoptotic bcl-2 and proapoptotic bax by RT-PCR were determined. E2 added in the coeliac ganglion caused an increase in the ovarian release of the P4, E2 and 3β-HSD, while in the ovary incubation alone it decreased P4 and 3β-HSD but increased and 20α-HSD and bax/bcl-2 ratio. It is concluded that through a direct effect on the ovary, E2 promotes luteal regression in DII rats, but the addition of E2 in the coeliac ganglion does not have the same effect. The peripheral nervous system, through the superior ovarian nerve, has a protective effect against the apoptotic mechanism on DII. © 2013 Elsevier Ltd.
Casais M.,CONICET |
Casais M.,Laboratorio Of Biologia Of La Reproduccion Labir |
Vallcaneras S.S.,CONICET |
Vallcaneras S.S.,Laboratorio Of Biologia Of La Reproduccion Labir |
And 8 more authors.
Reproductive Sciences | Year: 2012
There is evidence suggesting that estradiol (E2) regulates the physiology of the ovary and the sympathetic neurons associated with the reproductive function. The objective of this study was to investigate the effect of E2 on the function of late pregnant rat ovaries, acting either directly on the ovarian tissue or indirectly via the superior ovarian nerve (SON) from the celiac ganglion (CG). We used in vitro ovary (OV) or ex vivo CG-SON-OV incubation systems from day 21 pregnant rats. Various concentrations of E2 were added to the incubation media of either the OV alone or the ganglion compartment of the CG-SON-OV system. In both experimental schemes, we measured the concentration of progesterone in the OV incubation media by radioimmunoassay at different times. Luteal messenger RNA (mRNA) expression of 3?-hydroxysteroid dehydrogenase (3?-HSD) and 20?-hydroxysteroid dehydrogenase (20?-HSD) enzymes, respectively, involved in progesterone synthesis and catabolism, and of antiapoptotic B-cell lymphoma 2 (Bcl-2) and proapoptotic Bcl-2-associated X protein (Bax), were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) at the end of the incubation period. Estradiol added directly to the OV incubation or to the CG of the CG-SON-OV system caused a decline in the concentration of progesterone accumulated in the incubation media. In addition, E2, when added to the OV incubation, decreased the expression of 3?-HSD and the ratio of Bcl-2/Bax. We conclude that through a direct effect on the OV, E2 favors luteal regression at the end of pregnancy in rats, in association with neural modulation from the CG via the SON. © The Author(s) 2012.