Neuromodulation of the luteal regression: presence of progesterone receptors in coeliac ganglion

Abstract

New Findings r What is the central question of this study?The processes involved in luteal involution have not yet been clarified and, in general, have been studied only from a hormonal point of view. We investigated whether progesterone, from the coeliac ganglion through the superior ovarian nerve, is able to modify the luteal regression of late pregnancy in the rat. r What is the main finding and its importance?We showed that the luteal regression might be reversed by the neural effect of progesterone and demonstrated the presence of its receptors in the coeliac ganglion. This suggests that the peripheral neural pathway, through neuron-hormone interaction, represents an additional mechanism to control luteal function in addition to the classical endocrine regulation.The corpus luteum (CL) is a transitory endocrine gland that produces progesterone (P). At the end of its useful life, it suffers a process of functional and structural regression until its complete disappearance from the ovary. To investigate whether P is able to regulate the process of luteal regression through the peripheral neural pathway, we used the coeliac ganglion (CG)-superior ovarian nerve-ovary system from rats on day 21 of pregnancy. We stimulated the CG with P and analysed the functional regression through ovarian P release measured by radioimmunoassay, expression by RT-PCR and activity of luteal 3β-and 20α-hydroxysteroid dehydrogenase (anabolic and catabolic P enzymes, respectively). The luteal structural regression was evaluated through a study of apoptosis measured by TUNEL assay and the expression of apoptotic factors, such as Bcl-2, Bax, Fas and Fas ligand (FasL) by RT-PCR. To explore whether the effects mediated by P on the CL may be associated with P receptors, their presence in the CG was investigated by immunohistochemistry. In the group stimulated with P in the CG, the ovarian P release and the 3β-hydroxysteroid dehydrogenase activity increased, whereas the expression and activity of 20α-hydroxysteroid dehydrogenase decreased. In addition, a decrease in the number of apoptotic nuclei and a decrease of the expression of FasL were observed. We demonstrated the presence of P receptors in the CG. Overall, our results suggest that the regression of the CL of late pregnancy may be reprogrammed through the peripheral neural pathway, and this effect might be mediated by P bound to its receptor in the CG.

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

“…Besides, according to a relevant research, the inhibition of NF‐κB signaling pathway increased the anti‐apoptotic factor Bcl‐2 and decreased the pro‐apoptotic factors Bax and Fasl (Mattson, ). Bcl‐2, Bax, and Fasl were apoptosis‐related proteins, and their expressions influenced cell apoptosis (Ghersa et al, ). To further verify this role of the inhibition of NF‐κB signaling pathway, the present study analyzed the effect of this pathway on these apoptosis‐related factors.…”

Superior mesenteric ganglion neural modulation of ovarian angiogenesis, apoptosis and proliferation by the neuroactive steroid allopregnanolone

“…80 In the present study, SMG incubation with ALLO had an anti-apoptotic effect, significantly decreasing FAS-L ovarian mRNA expression. These results are similar to the reported effects of progesterone administration to an ex vivo CG-SON-ovary system, 84 where the treatment induced an anti-apoptotic effect through FAS-L decrease without changes in the BAX/BCL-2 ratio. ALLO thus may be involved in a part of progesterone actions because it has been suggested that some effects of progesterone might be mediated by active metabolites.…”