Control of the LH Receptor by Prolactin and Prostaglandin F2α in Rat Corpora Lutea

Grinwich, Daniel L.; Hichens, Martin; Behrman, Harold R.

doi:10.1095/biolreprod14.2.212

Cited by 106 publications

(22 citation statements)

References 19 publications

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“…LH receptors in swine and bovine corpora lutea have been reported to decrease immediately after PGF 2α administration [35,36] and continue to decline during the following 24 h; a similar trend has been reported, at least in swine, for both luteal and serum progesterone concentrations, so that all these parameters present a similar profile. The results from this study, on the contrary, indicate that both plasma and luteal P4 concentrations diminish before the reduction of LHr mRNA (which seems to be more related to the reduction in CL weight); these data are in agreement with those by Grinwich et al [37], who observed that the drop in luteal LH receptors in PGF 2α -treated rats is less pronounced than that of progesterone concentrations. Also Spicer et al [38] in the cow, Diekman et al [39] in the sheep and Roser et al [40] in the mare reported that the drop in blood progesterone levels precedes by several hours the drop in LH receptors or hCG binding sites in CL from PGF 2α -injected animals.…”

Section: Parameterssupporting

confidence: 92%

“…As suggested [38], the decrease in LH receptors does not seem to be the first step in corpora lutea regression which is likely associated to other events such as a direct antagonism of LH by PGF 2α [37]. These authors hypothesized that the very rapid effect of prostaglandins on progesterone secretion probably occurs through a reduction in the LH-induced hyperemic activity at the ovarian level; the loss of LH receptors possibly ensures the subsequent progression of the luteolytic process.…”

Section: Parametersmentioning

confidence: 92%

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Opposite regulation of clusterin and LH receptor in the swine corpus luteum during luteolysis

et al. 2003

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-Luteolysis, which occurs in a cyclical way to remove luteal tissue, may be an example of physiological apoptosis which counterbalances rapid tissue growth after ovulation. Clusterin is a multifunctional glycoprotein expressed in different tissues undergoing apoptosis. In this study we investigated clusterin and LH receptor gene expression during luteolysis as potential regulators of tissue growth and regression. Luteolysis was induced in pregnant sows (45 days) by Cloprostenol (PGF 2α analogue) treatment. Clusterin expression increased in the corpora lutea of pregnant sows ovariectomized 0, 6, 12, 24, 48 or 72 (n = 3) h after the luteolytic stimulus; maximum values were observed 24-48 h after the treatment (P < 0.01). An opposite trend between clusterin mRNA expression and markers of luteal function, such as progesterone levels in the corpora lutea and plasma, and LHr mRNA expression levels, was observed; moreover, clusterin expression was positively correlated with the degree of genomic DNA fragmentation, a marker of occurring apoptosis (P < 0.01). This pattern may be important in regulating luteolysis by a switch between luteotrophic and apoptotic stimulus. Our data indicate that P4 levels decrease prior to the increase in clusterin mRNA and the drop in LHr mRNA expression; we may therefore hypothesize a split between functional and structural luteolysis as reported in other species.LH receptor / tissue growth / clusterin / apoptosis / luteolysis

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Section: Parameterssupporting

confidence: 92%

Section: Parametersmentioning

confidence: 92%

Opposite regulation of clusterin and LH receptor in the swine corpus luteum during luteolysis

et al. 2003

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“…Thus, it can be argued that inhibition of hormone action may be the actual response to prostaglandins in luteal cells rather than the mediation of LH action in mouse ovarian tissue suggested by Kuehl et al (11). In vlvo, the ovary is constantly exposed to LH and, in the absence of this gonadotropin, luteal progesterone production rapidly wanes (16 (3) and in cultures of porcine, bovine, and human luteinized granulosa cells exposed to PGF2o, for several hours (18 (2,6). From the present data it is concluded that the rapid effect of PGF2 on progesterone secretion, which occurs in minutes, is due to inhibition of LH-dependent cAMP accumulation and not to inhibition of LH binding to its receptors.…”

Section: Discussionmentioning

confidence: 99%

“…Hichens et al (5) demonstrated such an action of PGF2< but, in later studies, Grinwich et al (6) found that the loss of LH receptors occurred several hours after the decrease in circulating progesterone. Thus, the loss of LH receptors may explain the long-term antigonadotropic action of PGF2,r in vio, but the acute action of PGF2<, appears to be independent of the number of LH binding sites in luteal tissue.…”

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confidence: 97%

Mechanism of the rapid antigonadotropic action of prostaglandins in cultured luteal cells

Thomas

Dorflinger

Behrman

1978

Proc. Natl. Acad. Sci. U.S.A.

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112

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A reproducible method for dissociation and culture of rat luteal cells is described. The concentration of LH required to produce half-maximal stimulation of progesterone secretion was 50 ng/ml. The effects of prostaglandin E2 (PGE2) and prostaglandin F2(PGF2a)on basal and luteinizing hormone (LH) 1344 chorionic gonadotropin (hCG) by corpora lutea in vivo coincident with a decrease in circulating progesterone within 30 min. However, interpretation of these data was confounded by possible effects of PGF2a on blood flow because PGF2a was found to produce a similar effect on luteal accumulation of 15I-labeled prolactin (7).To further examine the interaction between PGF2a and LH on luteal progesterone production, it was deemed important to study the early and direct actions of these agents on luteal cells in vitro. The present studies describe the effect of PGE2 and PGF2c, on LH-dependent progesterone secretion in conjunction with studies on the effect of PGF2. on binding of gonadotropin to isolated luteal cells in culture. In this same model the effect of simultaneous incubation of luteal cells with LH, dibutyryl cyclic AMP [(Bt)2-cAMPJ,' and theophylline in the presence and absence of PGF2a!, in addition to the effect of PGF2 and LH on adenylate cyclase and cAMP accumulation, was examined to provide information on the possible site of action of prostaglandins.MATERIALS AND METHODS Animals. Immature (26-day-old) rats (CD strain, Charles River Laboratories, Wilmington, MA) were given a subcutaneous injection of 50 international units (IU) of pregnant mare serum (Gestyl, Organon) followed, 64 hr later, by a second subcutaneous injection of 25 IU of hCG (A.P.L., Ayerst).Dispersion of Luteal Cells. Ovaries were removed 7 days after hCG injection, and the cells were dispersed in Ca2+-free medium (medium 1) (no. 138, GIBCO, Grand Island, NY) containing 2000 IU of collagenase (Worthington, Freehold, NJ) and 3M00 IU of deoxyribonuclease (Worthington) per g of tissue for 1 hr at 370 under 95% 02/5% CO2. The contents of the flask were filtered through nylon mesh (Nyten, Tetko Inc.) and centrifuged (5 min, 100 X g); the supernatant fraction was discarded and the pellet was washed three times with fresh medium 1. The final cell concentration (106 cells per ml) was made up in minimal essential medium with 25 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonate buffer and Earles's salts (medium 2) (no. 236, GIBCO). Cell numbers were determined with a hemocytometer, and cell viability was tested by the trypan blue dye test (8

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“…Some of the current studies which are germane to this area are: the effects of PGF2, upon LH receptor mechanisms (47), the role of estrogen in prostaglandin-induced luteolysis (48,49) as well as the direct effects of estradiol upon luteal cell progesterone secretion (50), and the role of lysosomes in luteal regression (51).…”

Section: Luteolytic Controlmentioning

confidence: 99%

Basic mechanisms of ovarian endocrine function

Schomberg¹

1978

Environ Health Perspect

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This review outlines the current understanding of ovarian endocrine development and regulation with both physiological and biochemical background to provide a framework applicable to problems concerning environmental agents and ovarian endocrine function. Two approaches are used. First, the endocrine regulation of foUicle development and corpus luteum function is considered in the classical sense, i.e., viewing these structures as gonadotropin-responsive units undergoing a programmed sequence of development and differentiation. Secondly, a relatively new area of ovarian physiology concerned with intra-ovarian regulation is explored, since this area holds potential for exploration of the direct effects of toxicological or environmental agents upon gonadal endocrine cells. Follicle DevelopmentGonadotropin-Independent and Dependent StagesThe stages of follicular maturation have been classified in a variety of ways by several different investigators, depending upon the degree of detail necessary (1, 2). For purposes of this discussion, distinction need only be made between the following: (1) the primordial follicle stage, characterized by an immature ovum surrounded by a single layer of flattened or disc-shaped granulosa cells; (2) the primary follicle stage, characterized by a transition in granulosa cell morphology to the cuboidal form followed by an increase in the number of granulosa cell layers (In the rat, oocyte growth is complete by the four-layer granulosa cell stage); and (3) Follicle development in most species, with the notable exception of the human (3), is thought to be independent of gonadotropic support up to the

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Control of the LH Receptor by Prolactin and Prostaglandin F2α in Rat Corpora Lutea

Abstract: Functional corpora lutea were induced in 28 day old, female rats with 4 iu of pregnant mare's serum, followed 72 h later with cervical

Cited by 106 publications

References 19 publications

Opposite regulation of clusterin and LH receptor in the swine corpus luteum during luteolysis

Opposite regulation of clusterin and LH receptor in the swine corpus luteum during luteolysis

Mechanism of the rapid antigonadotropic action of prostaglandins in cultured luteal cells

Basic mechanisms of ovarian endocrine function

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