Luteinizing Hormone, Prolactin and Ovarian 20α-Hydroxysteroid Dehydrogenase Levels during Pregnancy and Pseudopregnancy in the Rat123

Bast, Joseph D.; Melampy, R. M.

doi:10.1210/endo-91-6-1499

Cited by 85 publications

(37 citation statements)

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“…2), are in agreement with previous reports (Amenomori et al 1970;Denamur 1971;Bast and Melampy 1972;Linkie and Niswender 1972;Morishinge et al 1973;Nicholas and Hartmann 1981a) and with the changes observed in chronically cannulated rats (Fig. 1).…”

Section: Discussionsupporting

confidence: 93%

Progressive Changes in Plasma Progesterone, Prolactin and Corticosteroid Levels During Late Pregnancy and the Initiation of Lactose Synthesis in the Rat

Nicholas¹,

Hartmann²

1981

Aust. Jnl. Of Bio. Sci.

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The relationship between progesterone, prolactin, corticosteroids and corticosteroid binding globulin . (CBO) activity in plasma and the initiation of lactation were studied in normal parturient rats, and rats either ovariohysterectomized or Caesarean-sectioned on day 19 of gestation. In chronically cannulated rats the decline in plasma progesterone to low values « 10 p.g/l) in normal parturient rats 20 h before term and in Caesarean-sectioned rats 10--14 h after surgery was closely related to an increase in plasma prolactin. However, in ovariohysterectomized rats the levels of progesterone declined abruptly to 20 p.g/l within 30 min of surgery and prolactin remained low (5 p.g/l) for 4-8 h and then gradually increased during the subsequent 16-18 h. Lactose concentrations in mammary tissue of rats killed at 0, 12, 18. 24, 36 and 48 h after surgery was low « 0·14 mg/g tissue) up to 12 h, and increased to reach maximum values at 36 hand 48 h after surgery in ovariohysterectomized and Caesarean-sectioned rats respectively.The concentration of corticosteroids and CBO capacity in the plasma was 250--550 p.g/l and 250-480 p.g corticosterone bound per litre, respectively, in rats killed during the last 4 days of,gestation. However, both the concentration of corticosteroids and the CBO capacity, within the individual cannulated rats, remained relatively constant during late gestation.These findings support the proposal that progesterone withdrawal is the lactogenic trigger ana suggest the sequential involvement of prolactin. An increase in the concentration of free corticosteroids in late pregnancy and a related stimulatory role in the lactogenic mechanism were not established.

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Section: Discussionsupporting

confidence: 93%

Progressive Changes in Plasma Progesterone, Prolactin and Corticosteroid Levels During Late Pregnancy and the Initiation of Lactose Synthesis in the Rat

Nicholas¹,

Hartmann²

1981

Aust. Jnl. Of Bio. Sci.

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“…However, the results presented herein do not support such a conclusion. Indeed, PGF 2 ␣ can induce the expression of 20␣-HSD when administered on day 19 of pregnancy, a time when circulating levels of rat placental lactogen-2 are elevated (58,59) and when luteal PRL receptor is still highly expressed (57).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin F2α-induced Expression of 20α-Hydroxysteroid Dehydrogenase Involves the Transcription Factor NUR77

Stocco¹,

Zhong²,

Sugimoto³

et al. 2000

Journal of Biological Chemistry

120

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Prostaglandin F 2 ␣ (PGF 2 ␣) binding to its receptor on the rat corpus luteum triggers various signal transduction pathways that lead to the activation of a steroidogenic enzyme, 20␣-hydroxysteroid dehydrogenase (20␣-HSD), which in turn catabolizes progesterone. The molecular mechanism underlying PGF 2 ␣-induced 20␣-HSD enzyme activity has not yet been explored. In this report we show, using mice lacking PGF 2 ␣ receptor and pregnant rats, that PGF 2 ␣ is responsible for the rapid and massive expression of the 20␣-HSD gene at the end of pregnancy leading to a decrease in progesterone secretion. We also present evidence that PGF 2 ␣ enhances 20␣-HSD promoter activity. We have determined a region upstream of the ؊1590 position in the 20␣-HSD promoter that confers regulation by PGF 2 ␣ in ovarian primary cells. This region encompasses a unique transcription factor-binding site with a sequence of a NUR77 response element. Deletion of this motif or overexpression of a NUR77 dominant negative protein caused a complete loss of 20␣-HSD promoter activation by PGF 2 ␣. NUR77 also transactivated the 20␣-HSD promoter in transient transfection experiments in corpus luteumderived cells (GG-CL). This induction required the NUR77-transactivating domain. We also show that PGF 2 ␣ induces a very rapid expression of NUR77 that binds to a distal response element located at ؊1599/ ؊1606 but does not interact with another proximal putative NUR77 response element located downstream in the promoter. A rapid increase in NUR77 mRNA was observed in mice corpora lutea just before parturition at a time when 20␣-HSD becomes expressed. This increase in the expression of both genes was not seen in PGF 2 ␣ receptor knockout mice. By using cyclosporin A and PGF 2 ␣ treatment, we established that inhibition of NUR77 DNA binding in vivo prevents PGF 2 ␣ induction of the 20␣-HSD gene in the corpus luteum. Taken together, our results demonstrate, for the first time, that PGF 2 ␣ induces in the corpus luteum the expression of the nuclear orphan receptor and transcription factor, NUR77, which in turn leads to the transcriptional stimulation of 20␣-HSD, triggering the decrease in serum progesterone essential for parturition.In all mammalian species, progesterone plays an essential role in reproduction. The precise timing of both the synthesis and degradation of this steroid hormone is crucial for reproductive success. The expression of enzymes implicated in the synthesis and catabolism of progesterone, therefore, needs to be accurately regulated during the different reproductive states of the animal. In rodents, the corpus luteum, which is the only source of progesterone throughout pregnancy (1), is also able to express the enzyme 20␣-hydroxysteroid dehydrogenase (20␣-HSD)1 that converts progesterone into a biologically inactive steroid, thus playing a key role in the termination of pregnancy and allowing parturition to occur (2). Due to the detrimental effect of 20␣-HSD on luteal progesterone secretion, the corpus luteum of pregnancy does not express...

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“…They are initiated by uterine cervical stimulation accompanied by copulation [8]and are enhanced differentially by estradiol and progesterone [9]. Although these surges cease during the second half of pregnancy, a PRL surge occurs in the dark period preceding parturition [10, 11]. After parturition, a large amount of PRL is secreted in response to suckling stimuli, and high levels of serum PRL are maintained during 3 weeks of lactation [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Differential Regulation of Prolactin Release and Lactotrope Proliferation during Pregnancy, Lactation and the Estrous Cycle

Yin

2000

Neuroendocrinology

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The proestrous surge of prolactin (PRL) secretion and subsequent proliferation of lactotropes at estrus have been suggested to be induced by a common hypothalamic hormone. We investigated changes in lactotrope proliferation at other reproductive stages of female rats when PRL secretion was stimulated. To assess proliferative activity of lactotropes, incorporation of 5-bromo-2′-deoxyuridine (BrdU) into DNA was measured by double immunostaining for PRL and BrdU. BrdU-labeling indices, determined by BrdU injections at 10.00 h, revealed low levels of proliferative activity of lactotropes at the reproductive stages including diestrus, days 6 and 13 of pregnancy, and day 6 of lactation while high levels were detected on estrus and the day of parturition. When BrdU-labeling indices were determined at 3-hour intervals through day 6 of pregnancy to find an increase in lactotrope proliferation which might occur at times other than 10.00 h, proliferative activity of lactotropes remained at low levels with a slight increase in the afternoon. Such a diurnal change as observed in early pregnancy was not detected on day 13 of pregnancy. In contrast, short-interval determinations of BrdU-labeling indices during a period from day 20 of pregnancy to day 2 of lactation revealed a marked increase in proliferative activity on the day of parturition with a peak at 18.00 h, which was comparable to that observed at estrus. To investigate involvement of ovarian steroids in suppression of lactotrope proliferation as observed during early pregnancy and lactation, ovariectomized and pup-removed lactating rats were given one of treatment combinations of estradiol and suckling. In pup-removed lactating rats, estradiol treatment alone induced neither a PRL surge nor an increase in BrdU-labeling indices. Suckling stimuli, which were effective in increasing serum PRL concentrations irrespective of estradiol treatment, elicited a marked increase in BrdU-labeling indices in the presence of estradiol but not in its absence. These results suggest that proliferative activity of rat lactotropes does not necessarily correlate with PRL secretion during pregnancy and lactation. In contrast to PRL release, lactotrope proliferation requires both a hypophysiotropic stimulatory input from the hypothalamus and a sensitizing action of estradiol, an observation which may account for the fact that proliferation does not occur during pregnancy and lactation in spite of elevated PRL release.

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Luteinizing Hormone, Prolactin and Ovarian 20α-Hydroxysteroid Dehydrogenase Levels during Pregnancy and Pseudopregnancy in the Rat123

Cited by 85 publications

References 0 publications

Progressive Changes in Plasma Progesterone, Prolactin and Corticosteroid Levels During Late Pregnancy and the Initiation of Lactose Synthesis in the Rat

Progressive Changes in Plasma Progesterone, Prolactin and Corticosteroid Levels During Late Pregnancy and the Initiation of Lactose Synthesis in the Rat

Prostaglandin F2α-induced Expression of 20α-Hydroxysteroid Dehydrogenase Involves the Transcription Factor NUR77

Differential Regulation of Prolactin Release and Lactotrope Proliferation during Pregnancy, Lactation and the Estrous Cycle

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