Abstract
BackgroundMating changes the mechanism by which E2 regulates oviductal egg transport, from a non-genomic to a genomic mode. Previously, we found that E2 increased the expression of several genes in the oviduct of mated rats, but not in unmated rats. Among the transcripts that increased its level by E2 only in mated rats was the one coding for an s100 calcium binding protein G (s100 g) whose functional role in the oviduct is unknown.MethodsHerein, we investigated the participation of s100 g on the E2 genomic effect that accelerates oviductal transport in mated rats. Thus, we determined the effect of E2 on the mRNA and protein level of s100 g in the oviduct of mated and unmated rats. Then, we explored the effect of E2 on egg transport in unmated and mated rats under conditions in which s100 g protein was knockdown in the oviduct by a morpholino oligonucleotide against s100 g (s100 g-MO). In addition, the localization of s100 g in the oviduct of mated and unmated rats following treatment with E2 was also examined.ResultsExpression of s100 g mRNA progressively increased at 3-24 h after E2 treatment in the oviduct of mated rats while in unmated rats s100 g increased only at 12 and 24 hours. Oviductal s100 g protein increased 6 h following E2 and continued elevated at 12 and 24 h in mated rats, whereas in unmated rats s100 g protein increased at the same time points as its transcript. Administration of a morpholino oligonucleotide against s100 g transcript blocked the effect of E2 on egg transport in mated, but not in unmated rats. Finally, immunoreactivity of s100 g was observed only in epithelial cells of the oviducts of mated and unmated rats and it was unchanged after E2 treatment.ConclusionsMating affects the kinetic of E2-induced expression of s100 g although it not changed the cellular localization of s100 g in the oviduct after E2 . On the other hand, s100 g is a functional component of E2 genomic effect that accelerates egg transport. These findings show a physiological involvement of s100 g in the rat oviduct.
Highlights
Mating changes the mechanism by which E2 regulates oviductal egg transport, from a non-genomic to a genomic mode
Works have shown that antagonists of Endothelin receptor type A or B inhibited the effect of E2 on embryo transport [11] while Connexin 43 uncouplers blocked the increase in the instant velocity of microsphere movement induced by E2 in mated rats [12]
The Light Cycler instrument (Roche Diagnostics, GmbH Mannheim, Germany) was used to quantify the relative transcript level of s100 g, adenosine monophosphate deaminase 3 (Ampd3), Cyr61 and Tnfip6 while Gapdh was chosen as the housekeeping gene for load control because we have previously demonstrated that E2 or pregnancy did not affect its expression [9,12]
Summary
Mating changes the mechanism by which E2 regulates oviductal egg transport, from a non-genomic to a genomic mode. The transport of the gametes, fertilization or preimplantation development depends on the oviduct functions [1] In this context, the participation of ovarian hormones estradiol (E2) or progesterone (P) is crucial for the successful of these events. The duration of oviductal egg transport is dependent on ovarian hormones and mating-associated signals [3,4,5]. E2 accelerates egg transport to the uterus through intraoviductal genomic pathways in mated rats and through nongenomic pathways in unmated rats [3,7]. Both pathways require activation of estrogen receptors (ER) [8,9]. The E2 genomic pathway involves participation of endothelin receptors (ETR) and functional integrity of gap junctions in the oviduct
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