Participation of intraluteal progesterone and prostaglandin F2 alpha in LH-induced luteolysis in pregnant rat

Stocco, CO; Deis, R. P.

doi:10.1677/joe.0.1560253

Cited by 42 publications

(29 citation statements)

References 47 publications

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“…In addition, the ovarian administration of the hormone delays the decline in the activity of 3β-HSD during the functional regression of the CL, as well as the stimulation of the expression of 20α-HSD triggered by luteinizing hormone or prostaglandin F 2α (Stocco & Deis, 1998;Telleria et al 1999). Death of the luteal cells by apoptosis is the main cause of the CL structural regression (Stocco et al 2007).…”

Section: Discussionmentioning

confidence: 99%

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

Ghersa

Burdisso

Vallcaneras

et al. 2015

Experimental Physiology

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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.

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Section: Discussionmentioning

confidence: 99%

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

Ghersa

Burdisso

Vallcaneras

et al. 2015

Experimental Physiology

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“…4A). The dose of progesterone injected in the peripheral circulation elevates the level of circulating progesterone but does not elevate the level of progesterone in the CL to higher than normal in pregnant rats, which is approximately 80 ng/mg protein [31]. Prolactin, one of the main hormones involved in CL function in rats, did not change with treatment, displaying very low circulating levels in both vehicle-and progesterone-treated animals (Fig.…”

Section: Interference Of Structural Luteal Regression By Progesteronementioning

confidence: 90%

Progesterone Promotes Survival of the Rat Corpus Luteum in the Absence of Cognate Receptors1

Goyeneche

Deis

Gibori

et al. 2003

Biology of Reproduction

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Progesterone production by the corpus luteum (CL) is essential for preparation of the endometrium for implantation and for the maintenance of gestation. Progesterone modulates its own production and opposes functional luteal regression induced by exogenous agents, such as prostaglandin F(2alpha). In the present study, we evaluated whether progesterone is also capable of interfering with the process of structural luteal regression, which is characterized by a decrease in weight and size of the gland because of programmed cell death (i.e., apoptosis). We have found that a low number of luteal cells undergo apoptosis throughout gestation. On the day of parturition, but following the initial decline in endogenous progesterone production, a small increase in the number of luteal cells undergoing cell death was observed. This increase in apoptotic cells continued postpartum, reaching dramatic levels by Day 4 postpartum, and was accompanied by a marked decrease in average luteal weight. We have established that the exogenous administration of progesterone significantly reduces the decline in luteal weight observed during structural luteal regression postpartum. This effect was associated with a decrease in the number of cells undergoing apoptosis and with enhanced circulating levels of androstenedione. Furthermore, in vivo administration of progesterone delayed the occurrence of DNA fragmentation in postpartum CL incubated in serum-free conditions. Finally, we have shown that neither the CL of gestation nor the newly formed CL after postpartum ovulation express the classic progesterone-receptor mRNA. In summary, the present results support a protective action of progesterone on the function and survival of the CL through inhibition of apoptosis and stimulation of androstenedione production. Furthermore, this effect is carried out in the absence of classic progesterone receptors.

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“…It is also possible that the decrease in P 4 accumulation induced by LH is the result of an increase in 20␣-HSD activity. It is known that LH and cAMP increase the gene expression or activity of 20␣-HSD in rat granulosa cells [14,19,20]. However, it is important to note that in vivo, the increase in 20␣-HSD activity induced by LH occurs only 48 h after treatment; but the decrease in 3␤-HSD is observed as early as 8 h after LH treatment [14,20].…”

Section: Discussionmentioning

confidence: 99%

“…It is known that LH and cAMP increase the gene expression or activity of 20␣-HSD in rat granulosa cells [14,19,20]. However, it is important to note that in vivo, the increase in 20␣-HSD activity induced by LH occurs only 48 h after treatment; but the decrease in 3␤-HSD is observed as early as 8 h after LH treatment [14,20]. This long interval may indicate that after 6 h of incubation, the decrease in P 4 accumulation could be due to a decrease in P 4 synthesis instead of P 4 metabolism stimulation.…”

Section: Discussionmentioning

confidence: 99%

Luteinizing Hormone Inhibits Conversion of Pregnenolone to Progesterone in Luteal Cells from Rats on Day 19 of Pregnancy1

Stocco¹,

Deis²

1999

Biology of Reproduction

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We have previously reported that intrabursal ovarian administration of LH at the end of pregnancy in rats induces a decrease in luteal progesterone (P4) synthesis and an increase in P4 metabolism. However, whether this local luteolytic effect of LH is exerted directly on luteal cells or on other structures, such as follicular or stromal cells, to modify luteal function is unknown. The aim of the present study was to determine the effect of LH on isolated luteal cells obtained on Day 19 of pregnancy. Incubation of luteal cells with 1, 10, 100, or 1000 ng/ml of ovine LH (oLH) for 6 h did not modify basal P4 production. The addition to the culture medium of 22(R)-hydroxycholesterol (22R-HC, 10 microgram/ml), a membrane-permeable P4 precursor, or pregnenolone (10(-2) microM) induced a significant increase in P4 accumulation in the medium in relation to the control value. When luteal cells were preincubated for 2 h with oLH, a significant (p < 0.01) reduction in the 22R-HC- or pregnenolone-stimulated P4 accumulation was observed. Incubation of luteal cells with dibutyryl cAMP (1 mM, a cAMP analogue) plus isobutylmethylxanthine (1 mM, a phosphodiesterase inhibitor) also inhibited pregnenolone-stimulated P4 accumulation. Incubation with an inositol triphosphate synthesis inhibitor, neomycin (1 mM), or an inhibitor of intracellular Ca2+ mobilization, (8,9-N, N-diethylamino)octyl-3,4,5-trimethoxybenzoate (1 mM), did not prevent the decrease in pregnenolone-stimulated P4 secretion induced by oLH. It was concluded that the luteolytic action of LH in late pregnancy is due, at least in part, to a direct action on the luteal cells and that an increase in intracellular cAMP level might mediate this effect.

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Participation of intraluteal progesterone and prostaglandin F2 alpha in LH-induced luteolysis in pregnant rat

Cited by 42 publications

References 47 publications

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

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

Progesterone Promotes Survival of the Rat Corpus Luteum in the Absence of Cognate Receptors1

Luteinizing Hormone Inhibits Conversion of Pregnenolone to Progesterone in Luteal Cells from Rats on Day 19 of Pregnancy1

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