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Biology of Reproduction 60, 729-732 (1999)
©Copyright 1999 Society for the Study of Reproduction, Inc.

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

Carlos O. Stocco2,a, and Ricardo P. Deis3,a

a Laboratorio de Reproducción y Lactancia, LARLAC-CONICET, 5500 Mendoza, Argentina


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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 µg/ml), a membrane-permeable P4 precursor, or pregnenolone (10-2 µM) 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.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
LH is essential to sustain corpus luteum (CL) function during the first half of pregnancy in rats [1–4], while after Day 12 of pregnancy, LH and the pituitary are not necessary to maintain progesterone (P4) production [5, 6]. However, the increase in plasma LH levels at the end of pregnancy could be correlated with the physiological process of luteolysis preceding parturition [7–9]. Rothchild in an early paper provided the first evidence that LH may promote luteolysis in hypophysectomized rats [10]. During the terminal stages of pregnancy and pseudopregnancy, a positive correlation has been observed between serum LH levels and ovarian 20{alpha}-hydroxysteroid dehydrogenase (20{alpha}-HSD) activity [11]. 20{alpha}-HSD is an enzyme that converts P4 into a derivative devoid of progestational activity and is considered a marker of luteolysis [11–13]. We have recently shown that the intrabursal administration of an antiserum against rat LH on Day 19 of pregnancy prevents the increase in 20{alpha}-HSD activity and the consequent fall in serum P4 levels observed on Day 21 of pregnancy [14]. Moreover, we have demonstrated that the intrabursal administration of ovine LH on Day 19 of pregnancy induces an increase in 20{alpha}-HSD activity and a decrease in 3ß-HSD activity [14]. 3ß-HSD is an enzyme that catalyses the formation of P4 from pregnenolone [1]. These results have established an important role of LH during the luteolytic process in rats. However, it is not known whether the local effect of intrabursal administration of LH is exerted directly on luteal cells or on other structures, such as follicular or stromal cells, to modify luteal function. The aim of this work was to examine the effect of LH on P4 synthesis in an in vitro model of dispersed luteal cells, obtained from Day 19 pregnant rats, in order to determine whether LH has a direct luteolytic effect on these cells. An additional objective was to determine the secondary messenger system involved in the action of LH on luteal function at the end of pregnancy.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Animal

Pregnant rats bred in our laboratory (originally Wistar strain, Day 0 = sperm positive), with free access to standard rat chow (Cargill, Santa Fe, Argentina) and water and kept under controlled conditions of light (lights-on from 0600 to 2000 h) and temperature (22–24ÅC), were used throughout this study.

Materials

[1,2,6,7-3H]Progesterone (98 Ci/mmol) was purchased from Amersham Life Science (Buckinghamshire, UK). Collagenase (type IV, 160 U/mg), neomycin, TMB-8 (8,9-[N,N-diethylamino]octyl-3,4,5-trimethoxybenzoate), dibutyryl cAMP (dbcAMP), 22(R)-hydroxycholesterol (22R-HC), isobutylmethylxanthine (IBMX), Hanks' balanced salt solution (HBSS), McCoy's 5A medium, Ham's F-12 nutrient mixture, and pregnenolone (P5) were purchased from Sigma Chemical Co. (St. Louis, MO). Dispase (type II, 0.5 U/mg) and DNase (2000 U/mg) were purchased from Boehringer-Mannheim Biochemicals (Indianapolis, IN). Ovine LH (oLH-26) was provided by NIDDK (Bethesda, ND). Other reagents and chemicals were of analytical grade. Luteal cells were incubated in 24-well plastic tissue culture dishes (Corning Laboratory Sciences Co., Corning, NY).

Luteal Cell Dispersion

For cell isolation, we used the methods described by Nelson et al. [15]. For each luteal cell dispersion, CL were pooled from at least 9 rats. Briefly, on Day 19 of pregnancy, rats were anesthetized with ether, and ovaries were dissected out. They were placed in HBSS containing 2% BSA and 25 mM Hepes, pH 7.4. Any follicle adhering to the CL was carefully removed. CL were incubated at 37ÅC with 50 U/ml collagenase, 2.4 U/ml dispase, and 200 U/ml DNase in four consecutive incubations (30 min each), with stirring at 100 rpm under an atmosphere of 100% O2. After each incubation, the cells were centrifuged at 200 x g, the supernatant was discarded, and fresh medium and enzymes were added. At the end of enzyme treatment, CL were treated for 15 min in 10 ml EDTA solution (0.02% EDTA w:v in PBS) containing 2% BSA and 25 mM Hepes, pH 7.4. After this treatment, the cells were centrifuged at 200 x g. The new pellet was resuspended in 10 ml of dissection medium and filtered through nylon mesh. The viability was approximately 90% as determined by trypan blue staining. For all experiments, luteal cells were cultured at 37ÅC under an atmosphere of 95% air:5% CO2 using 105 viable cells per milliliter of culture medium (McCoy's 5A:Ham's F-12, 1:1). At the end of each experiment, the cells were centrifuged, and the culture medium was frozen at -20ÅC for subsequent RIA of P4.

P4 RIA

P4 was assayed in unextracted incubation medium using an RIA developed in our laboratory with an antiserum raised against P4-11-BSA conjugate in rabbits. The sensitivity and variability of this RIA have been previously reported [16]. The antiserum to P4 cross-reacted 100% with P4 and 0.05% with pregnenolone. The P4 concentration was not detectable in culture medium alone and was 19.66 ± 0.93 ng/ml in culture medium containing 10-2 mM pregnenolone.

Statistical Analysis

All results are given as the mean ± SEM of quadruplicate determinations and are representative of three different experiments. Statistical comparisons were made by one-way ANOVA (ANOVA I) followed by Tukey test using Prism (GraphPad Software, San Diego, CA). A value of p < 0.05 was considered significant.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Effect of oLH on P4 Production by Luteal Cells Obtained from Rats on Day 19 of Pregnancy (Fig. 1)

Luteal cells obtained from rats on Day 19 of pregnancy were incubated for 6 h in culture medium in the absence or presence of various concentrations of oLH (1, 10, 100, or 1000 ng/ml). As shown in Figure 1, the various doses of oLH did not modify basal P4 accumulation.



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  		FIG. 1. P4 accumulation by luteal cells obtained from 19-day-pregnant rats in the presence or absence of various concentrations of oLH. Values are the mean ± SEM of quadruplicate determinations in three separate experiments.

Effect of oLH on P450 Side-Chain Cleavage (P450scc) and 3ß-HSD Activities (Fig. 2)

The effect of LH on P450scc and 3ß-HSD activities was estimated by conversion of 22R-HC or pregnenolone to P4, respectively [17]. In luteal cells initially incubated in the absence of oLH for 2 h, the addition of 22R-HC (10 µg/ml) or pregnenolone (10-2 mM) for the next 4 h induced a significant increase in the concentration of P4 in the medium when compared with basal P4 accumulation. However, when luteal cells were preincubated for 2 h with oLH (1000 ng/ml), the 22R-HC- or pregnenolone-induced increase in P4 accumulation was significantly reduced (p < 0.01).



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  		FIG. 2. Effect of oLH (1000 ng/ml) on 22R-HC- or pregnenolone-stimulated P4 production in luteal cells obtained from rats on Day 19 of pregnancy. Dotted line indicates basal P4 accumulation: 25 ± 3.15 ng/105 cells per 6 h. Values are the mean ± SEM of quadruplicate determinations in three separate experiments; p < 0.01 indicates the degree of significance of the difference between columns; ANOVA I, Tukey test.

Effect of cAMP, Neomycin, and TMB-8 on Pregnenolone-Induced P4 Accumulation (Fig. 3, Table 1)

Incubation of luteal cells from Day 19 of pregnancy with dbcAMP (1 mM) plus IBMX (1 mM) for 6 h did not modify basal P4 production. However, when luteal cells were preincubated for 2 h with dbcAMP plus IBMX, the increase in P4 accumulation induced by the addition of pregnenolone for the following 4 h was significantly reduced (p < 0.01) (Fig. 3).



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  		FIG. 3. Effect of dbcAMP and IBMX (MIX) on pregnenolone-stimulated P4 accumulation in luteal cells obtained from rats on Day 19 of pregnancy. Basal: 28 ± 2.85 ng/105 cells per 6 h. Values are the mean ± SEM of quadruplicate determinations in three separate experiments. The columns with different letters are significantly different; ANOVA I, Tukey test.


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  		TABLE 1. Progesterone production (ng/105 cells per 6 h) by luteal cells from 19-day-pregnant rats: effect of incubation with an IP3 synthesis inhibitor, neomycin, or an inhibitor of intracellular Ca2+ mobilization, TMB-8, on the inhibition of pregnenolone-stimulated P4 secretion induced by oLH.*

Luteal cells from Day 19 pregnant rats were incubated for 2 h in culture media in the absence or presence of oLH (1000 ng) plus neomycin (1 mM) or TMB-8 (1 mM); pregnenolone (10-2 M) was then added to the medium for the next 4 h of incubation. Preincubation of luteal cells for 2 h with neomycin (1 mM) or TMB-8 (1 mM) did not modify the increase in P4 accumulation induced by pregnenolone (10-2 M). When luteal cells were preincubated for 2 h in the presence of oLH (1000 ng/ml) plus neomycin or TMB-8, the decrease in the pregnenolone-stimulated P4 accumulation induced by oLH was not modified (Table 1).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Ours results show that basal P4 accumulation is not modified by incubation of rat luteal cells from Day 19 of pregnancy with different doses of oLH or agents that increase intracellular cAMP. These in vitro results are in agreement with previous in vivo studies indicating that LH is not necessary for the maintenance of luteal function during the second half of pregnancy [5, 6], in contrast to the clear luteotropic effect of LH/cAMP in the first half of pregnancy [1, 3]. Moreover, using 22R-HC, a membrane-permeable P4 precursor [18], and pregnenolone to monitor P450scc and 3ß-HSD activities, respectively, we found that conversion of 22R-HC and pregnenolone to P4 was significantly reduced by LH. These results may indicate that the luteolytic effects of LH on late-pregnant rats, previously demonstrated in vivo [14], is due at least in part to a direct action on luteal cells. Furthermore, these results also indicate that this effect of LH could be mediated by a decrease in P450scc and/or 3ß-HSD activities. It is also possible that the decrease in P4 accumulation induced by LH is the result of an increase in 20{alpha}-HSD activity. It is known that LH and cAMP increase the gene expression or activity of 20{alpha}-HSD in rat granulosa cells [14, 19, 20]. However, it is important to note that in vivo, the increase in 20{alpha}-HSD activity induced by LH occurs only 48 h after treatment; but the decrease in 3ß-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 P4 accumulation could be due to a decrease in P4 synthesis instead of P4 metabolism stimulation.

We did not observe a reduction of basal P4 accumulation in the presence of oLH, despite decreased conversion of pregnenolone to P4 induced by this hormone. This lack of correlation between P4 secretion and luteal 3ß-HSD activity was also observed in previous studies. Thus, treatment with LH on Day 19 of pregnancy induced an early decrease in 3ß-HSD activity followed by a reduction in intraluteal P4 content, both of which occurred prior to the increase in 20{alpha}-HSD activity and luteal PGF2{alpha} content and to the decrease in serum P4 levels [14, 20]. In addition, recent evidence indicates that P4 prevents the increase in 20{alpha}-HSD activity [20] or, acting through the glucocorticoid receptor, down-regulates its expression [21]. Therefore, it is likely that the decrease in the conversion of pregnenolone to P4 initially affects only the intracellular levels of P4, which in turn trigger an increase in 20{alpha}-HSD activity.

It is well established that the binding of LH/hCG to the LH receptor results in the activation of adenyl cyclase and the production of cAMP [22, 23]. In agreement with this, we found that pregnenolone-stimulated P4 production was inhibited when luteal cells were incubated with dbcAMP, which is a membrane-permeable cAMP analogue [24], and IBMX, a phosphodiesterase inhibitor [25]. This result suggests that the luteolytic effect of LH might be exerted through an increase in intracellular cAMP. However, further studies are necessary to define the participation of cAMP.

There is evidence that multiple signal transduction pathways are involved in mediating the cellular actions of LH. Studies with cultured rat granulosa cells [26] and isolated bovine luteal cells [27] provide strong evidence that LH activates not only the protein kinase A pathway but also the protein kinase C, raising intracellular levels of inositol triphosphate (IP3) and/or Ca2+. We explored whether these second messengers mediate the luteolytic effect of LH by incubating luteal cells with LH plus TMB-8, a putative calcium antagonist [28, 29], or plus neomycin, an inhibitor of IP3 formation [30, 31]. It is interesting to note that the inhibition of IP3 synthesis or intracellular Ca2+ mobilization did not modify the effect of LH on the conversion of pregnenolone to P4, indicating that these second messengers may not be directly involved in the luteolytic effect of LH.

A striking feature of the rat model is that the regulation of P4 secretion is related to the endocrine status of the animals studied [1]. Results from our laboratory and from others indicate that LH may participate in this differential regulation of P4 synthesis throughout pregnancy. Thus, LH [2–4] and cAMP [3] induce an increase in the synthesis and secretion of P4 during the first part of pregnancy but have an inhibitory effect at the end of pregnancy [14, 30,32]. One important question, with respect to these opposing effects of LH, is why this gonadotropin has such divergent action. One likely answer is provided by analysis of the different levels of LH throughout pregnancy. During the first part of pregnancy, LH levels are constant but low. However, after Day 19 of pregnancy, there is an abrupt increase in circulating LH [2, 33]. This high level of LH could be implicated in the luteolysis occurring at the end of pregnancy. It has recently been shown in vivo that the high levels of LH reached during the proestrus LH surge induce the expression of a protein called inducible cAMP early repressor (ICER), which is a member of the cAMP response element modulatory protein family. ICER is implicated in the repression of inhibin {alpha}-subunit expression in rat granulosa cells [34]. We have also recently demonstrated, in a dose-response experiment, that only high doses of LH administered intrabursally (4 or 8 µg/ovary) provoked a decrease in 3ß-HSD activity [14]. Although it is difficult to compare doses used in vitro with in vivo circulating levels, it seems reasonable to speculate that at the end of pregnancy the LH surge may induce repression of 3ß-HSD gene expression, particularly when one considers both the present and previous in vivo studies.


   ACKNOWLEDGMENTS
 
The authors are grateful to NIH for the generous supply of oLH.


   FOOTNOTES
 
1 This work was supported by grant No. PMT-PICT0098 from Agencia Nacional de Promoción Científica y Tecnológica and by grant PLI 325/8 PRE 023/98 from the PLACIRH (Programa Latinoamericano de Capacitación e Investigación en Reproducción Humana). Back

2 Correspondence and current address: Department of Physiology and Biophysics (M/C 901), University of Illinois at Chicago, 835 South Wolcott Avenue, Chicago, IL 60612–7342. FAX: 312 413 0159; costocco{at}tigger.uic.edu Back

3 Reprint requests: Ricardo P. Deis, Laboratorio de Reproducción y Lactancia, LARLAC-CONICET Casilla de Correo 855, 5500 Mendoza, Argentina. FAX: 54-61-273976; LarLac{at}Lab.cricyT.edu.ar Back

Accepted: October 20, 1998.

Received: April 29, 1998.


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 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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