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PubMed1987

Plasma prolactin response to submaximal stimulation by TRH and endogenous corticosteroids in man.

Recent studies suggest that submaximal plasma prolactin responses to TRH may reflect the effects of endogenous dopamine on prolactin release more accurately than basal plasma prolactin levels or maximal plasma prolactin responses to TRH. In the present study the plasma prolactin response to 12.5 micrograms i.v. TRH in 25 male subjects was significantly correlated with 24-hour urinary 17-ketogenic steroid excretion (= "total" 17-hydroxy corticosteroids). With regard to the basal plasma prolactin level or the prolactin response to 200 micrograms i.v. TRH, no such relation with corticosteroid excretion was detected. It is concluded that the plasma prolactin response to 12.5 micrograms i.v. TRH may provide a new, useful investigative tool with which to study corticosteroid-dopamine interactions and central dopamine activity in man.

17-Hydroxycorticosteroids↗
PubMed1985

Submaximal plasma prolactin response to TRH and dopamine activity in man.

Submaximal plasma prolactin responses to TRH were evaluated as a measure of endogenous dopamine activity in man. In 25 male subjects, plasma prolactin responses to 0.5 mg i.m. haloperidol were significantly correlated with plasma prolactin responses to 12.5 micrograms i.v. TRH but not with plasma prolactin responses to 200 micrograms i.v. TRH or with basal plasma prolactin levels. The results suggest that submaximal plasma prolactin responses to TRH may reflect the effects of endogenous dopamine activity on prolactin release more accurately than the prolactin measures previously used.

Adult↗
PubMed1987

[Stimulation of prolactin secretion by vasoactive intestinal peptide].

Dopamine has already been recognized as an inhibiting factor of prolactin. On the other hand, the stimulators of prolactin are still judged diversely at the moment. In addition to hypothalamic TRH, serotonine as well as endogenous opiates and VIP are under discussion. The object of our studies was testing the function of VIP in directing prolactin secretion on three different groups of patients: 1. hyperprolactinaemic women of WHO-group VI; 2. patients who had undergone a TRH-test along with an endocrine check-up; 3. post partum in childbed. The determination was made from analyzing peripheral blood by radioimmunoassay. In 20 amenorrhoeic patients of WHO-group VI, their prolactin and VIP levels were determined between 8 and 10 a. m. Only 4 patients showed a VIP-concentration below 20 pg/ml (which represents the limit of detectability). The other 16 patients showed an increased concentration of VIP. In 15 cases there was an obvious correlation of VIP and prolactin concentrations according to the linear regression. In the course of a TRH-test to 20 and 40 minutes after initial blood examination prolactin and VIP were again determined. After 20 minutes all patients showed a threefold increase of the initial prolactin value. On the other hand, VIP increased in 3 cases only. Apart from all those patients who wanted to become pregnant, these three women--being postmenopausal--showed increased initial values already in the unstimulated condition. The third group of patients consisted of 26 women in childbed. Their prolactin and VIP were determined between the second and eight day post partum.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1986

Changes in prolactin in peripheral plasma during lactation in the brushtail possum Trichosurus vulpecula.

A heterologous double-antibody radioimmunoassay has been validated for prolactin in plasma and pituitary preparations of T. vulpecula. Serial dilutions of crude pituitary homogenates and plasmas from several marsupials and purified prolactin from the tammar, Macropus eugenii, showed parallel dose response curves. In both male and female possums plasma prolactin concentrations increased in response to a single intravenous injection of thyrotrophin releasing hormone. Plasma prolactin concentrations were measured in six lactating females (June-November) and in four non-lactating females (July-October). In the following year prolactin levels were also measured in 11 possums with young less than 50 days old and in 24 possums with young aged between 100 and 145 days. In early lactation prolactin concentrations were low (less than 8 ng/ml) but increased to high levels (greater than 30 ng/ml) by 120 days and remained high until about 160 days of lactation. Thereafter concentrations declined although the young continued to take milk from the mother for a further 30-50 days. The changes in plasma prolactin concentrations throughout lactation are very similar to those described for the tammar, and this unusual pattern appears to be common to marsupials. Non-lactating possums showed no consistent changes in plasma prolactin concentrations between July and October.

Animals↗
PubMed1998

Galanin regulates prolactin release and lactotroph proliferation.

The neuropeptide galanin is predominantly expressed by the lactotrophs (the prolactin secreting cell type) in the rodent anterior pituitary and in the median eminence and paraventricular nucleus of the hypothalamus. Prolactin and galanin colocalize in the same secretory granule, the expression of both proteins is extremely sensitive to the estrogen status of the animal. The administration of estradiol-17beta induces pituitary hyperplasia followed by adenoma formation and causes a 3,000-fold increase in the galanin mRNA content of the lactotroph. To further study the role of galanin in prolactin release and lactotroph growth we now report the generation of mice carrying a loss-of-function mutation of the endogenous galanin gene. There is no evidence of embryonic lethality and the mutant mice grow normally. The specific endocrine abnormalities identified to date, relate to the expression of prolactin. Pituitary prolactin message levels and protein content of adult female mutant mice are reduced by 30-40% compared with wild-type controls. Mutant females fail to lactate and pups die of starvation/dehydration unless fostered onto wild-type mothers. Prolactin secretion in mutant females is markedly reduced at 7 days postpartum compared with wild-type controls with an associated failure in mammary gland maturation. There is an almost complete abrogation of the proliferative response of the lactotroph to high doses of estrogen, with a failure to up-regulate prolactin release, STAT5 expression or to increase pituitary cell number. These data further support the hypothesis that galanin acts as a paracrine regulator of prolactin expression and as a growth factor to the lactotroph.

Alleles↗
PubMed1998

Receptor-like protein-tyrosine phosphatase alpha specifically inhibits insulin-increased prolactin gene expression.

A physiologically relevant response to insulin, stimulation of prolactin promoter activity in GH4 pituitary cells, was used as an assay to study the specificity of protein-tyrosine phosphatase function. Receptor-like protein-tyrosine phosphatase alpha (RPTPalpha) blocks the effect of insulin to increase prolactin gene expression but potentiates the effects of epidermal growth factor and cAMP on prolactin promoter activity. RPTPalpha was the only protein-tyrosine phosphatase tested that did this. Thus, the effect of RPTPalpha on prolactin-chloramphenicol acetyltransferase (CAT) promoter activity is specific by two criteria. A number of potential RPTPalpha targets were ruled out by finding (a) that they are not affected or (b) that they are not on the pathway to insulin-increased prolactin-CAT activity. The negative effect of RPTPalpha on insulin activation of the prolactin promoter is not due to reduced phosphorylation or kinase activity of the insulin receptor or to reduced phosphorylation of insulin receptor substrate-1 or Shc. Inhibitor studies suggest that insulin-increased prolactin gene expression is mediated by a Ras-like GTPase but is not mitogen-activated protein kinase dependent. Experiments with inhibitors of phosphatidylinositol 3-kinase suggest that insulin-increased prolactin-CAT expression is phosphatidylinositol 3-kinase-independent. These results suggest that RPTPalpha may be a physiological regulator of insulin action.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed2001

Elk-1, C/EBPalpha, and Pit-1 confer an insulin-responsive phenotype on prolactin promoter expression in Chinese hamster ovary cells and define the factors required for insulin-increased transcription.

The transcription factor(s) that mediate insulin-increased gene transcription are not well defined. These studies use phenotypic conversion of Rat2 and Chinese hamster ovary (CHO) cells with transcription factors to identify components required for regulation of prolactin promoter activity and its control by insulin. The pituitary-derived GH4 cells contain all of the transcription factors required for insulin-increased prolactin-chloramphenicol acetyltransferase (CAT) expression while HeLa cells require only Pit-1, a pituitary-specific factor. However, Rat2 and CHO cells require additional factors. We had determined previously that the transcription factor that mediates insulin-increased prolactin gene expression was likely an Ets-related protein. Elk-1 and Sap-1 were the only Ets-related transcription factors tested as chimeras with LexA DNA-binding domain that were able to mediate insulin-increased expression of a LexA-CAT reporter plasmid. Elk-1 and Sap-1 are expressed in GH4 and HeLa cells but Rat2 and CHO cells express Sap-1, but not Elk-1. Expression of Elk-1 made Rat2 cells (but not CHO cells) insulin responsive. C/EBPalpha also binds to the prolactin promoter at a sequence overlapping the binding site for Elk-1. Expression of both C/EBPalpha and Pit-1 in CHO cells is required for high basal transcription of prolactin-CAT. Expression of Elk-1 converts CHO cells into a phenotype in which prolactin gene expression is increased by insulin treatment. Finally, antisense mediated reduction of Elk-1 in GH4 cells decreased insulin-increased prolactin gene expression and confirmed the requirement for Elk-1 for insulin-increased prolactin gene expression. Thus, both C/EBPalpha and Pit-1 were required for high basal transcription while insulin sensitivity required Elk-1.

3T3 Cells↗
PubMed1999

Routing, processing and export of rat pituitary prolactin: identification of a 36 kDa disulphide-bridged oligomeric preprolactin.

To gain an insight in the routing, processing and export of rat prolactin, rat pituitary cells were cultured in serum-free medium in the presence of cycloheximide, carbonyl cyanide m-chlorophenylhydrazone, Brefeldin A and monensin. The potential influence of these perturbants, whose well documented effects are the altering of protein synthesis and transport, was studied on rat prolactin molecular size isoforms appearing in cellular extracts and in culture medium. The outcome of the culture experiments as recorded in vertical SDS-PAGE, thiol gradient electrophoresis and sequential SDS-PAGE followed by prolactin specific immunoblotting and densitometry, was as follows: (1) at the cellular level we were able to characterize a novel 36 kDa protein as a disulphide-bridged oligomeric precursor prolactin, which is presumably rapidly transformed in the cis/medial Golgi; to designate monomeric rat prolactin as an early Golgi protein and t o advance evidence that the main processing of the glycosylated rat prolactin is a cis/medial Golgi event; (2) in release none of the perturbants disturbed the relative distribution of monomeric and glycosylated rat prolactin, the main molecular size isoforms currently secreted by untreated pituitary cells, or induced the appearance of transformed molecular size isoforms; (3) the secretion mode indicates that rat prolactin is released via the regulated pathway in the presence of the perturbants used.

Animals↗
PubMed2004

Serum and seminal plasma prolactin levels in male attenders of an infertility clinic in Ibadan.

Serum and seminal plasma prolactin and testosterone were studied in 51 healthy-looking men who presented at the infertility clinic. They included 20 men with normospermia, 20 with oligospermia and 11 with azoospermia. The mean serum prolactin and gonadotrophin levels of the oligospermics and azoospermics were similar but significantly higher than those of the normospermics. The mean seminal plasma prolactin levels in the three groups were similar. The mean serum testosterone of the azoospermics was significantly higher than those of the oligospermics and normospermics who had similar levels. The seminal plasma testosterone of the oligospermics was similar to that of the azoospermics but significantly higher than that of the normospermics. A significant correlation occurred between serum prolactin and sperm motility. No correlation occurred between the serum and seminal plasma prolactin levels, and seminal plasma testosterone or between serum and seminal plasma testosterone. Seminal prolactin has no correlation with any biophysical parameters. It was concluded that poor spermatogenesis is associated with high serum prolactin in patients with infertility. Serum but not seminal plasma prolactin assay is useful in assessing male infertility.

Adult↗
PubMed1982

Prolactin storage in a clonal strain of rat pituitary tumor cells is cell-cycle dependent.

GH4C1 cells (CH cells) are a clonal strain of rat pituitary tumor cells which secrete prolactin. We measured intracellular prolactin at different stages of the cell cycle using flow microfluorometry. Prolactin was stained by an indirect immunocytochemical technique using fluorescein isothiocyanate (FITC)-conjugated antiserum, and DNA was stained simultaneously with propidium iodide. We found that prolactin storage in GH cells was cell-cycle dependent; prolactin storage increased as cells passed from G1 to S to G2 + M. We have shown previously that insulin and 17 beta-estradiol act synergistically to increase intracellular prolactin three- to sevenfold and slow the rate of cell growth to approximately 70% of control cells. In this study we observed that insulin and estradiol increased prolactin storage at each stage of the cell cycle but did not affect the cell-cycle distribution of the population even though cell growth was slowed. We conclude that insulin and estradiol did not increase prolactin storage by affecting the cell-cycle distribution of the population.

Animals↗
PubMed2003

Prolactin acts as a potent survival factor against C2-ceramide-induced apoptosis in human granulosa cells.

BACKGROUND: The role of prolactin in the regulation of ovarian folliculogenesis and corpus luteal function and in particular its relationship to atresia in these structures is as yet unclear. We established a model of apoptosis in which to examine the actions of prolactin. METHOD: Granulosa cells collected from IVF-flush were cultured at 0.1-0.3 x 10(6) cells/well in growth media for 48 h, placed into serum-free media for 24 h prior to dosing for 24 h. Dose responses to C2-ceramide and prolactin were performed. Cells were then treated with an apoptotic dose of C2-ceramide alone, prolactin (100 ng/ml) alone or a combination of the two. Cell death was assessed by Trypan Blue cell counting and MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Thiazolyl Blue] assay and apoptosis confirmed by morphological assessment and flow cytometry. RESULTS: C2-ceramide (0-40 micro mol/l) induced a dose-dependent increase in cell death (63.8% increase at 40 micro mol/l) and, morphologically, cells exhibited classical features of apoptosis. Prolactin alone had no effect on metabolic activity or total cell number. On co- incubation, prolactin alone had no effect on cell death, whereas C2-ceramide induced an approximately 62.6% increase in apoptosis, which was inhibited in the presence of prolactin. CONCLUSIONS: Prolactin may contribute significantly to early corpus luteum formation and survival by acting as a potent antiapoptotic factor for human granulosa cells.

Apoptosis↗
PubMed1993

Excessive and dysregulated secretion of prolactin in rheumatoid arthritis: immunopathogenetic and therapeutic implications.

Prolactin (PL) is essential for the normal function of the immune system. It is required for the induction of a number of autoimmune conditions in experimental animals. The role of prolactin in the immunopathogenesis of autoimmune human disease has not been established. RA is characterized by a variety of immune and inflammatory processes which determine disease activity. It has a pronounced diurnal periodicity with a peak at 03.15 hours. Since PL has a diurnal rhythm of secretion in man with a peak at about 02.00 hours, it may contribute to the nocturnal worsening of RA. We show that patients with RA secrete an excess of prolactin as evidenced by an upregulated diurnal periodicity and an abnormal increase in plasma prolactin concentration following surgery. By contrast, patients with chronic osteomyelitis, who had chronic inflammation of similar severity to patients with RA, had a normal prolactin diurnal rhythm and response to surgery. Hence, the abnormal changes in prolactin physiology seen in RA appear to be a feature of the disease per se rather than related to chronic inflammation. The elevated levels of prolactin may contribute to disease activity by augmenting immune processes and may be an additional genetic factor, independent of HLA-DR4, in the immunopathogenesis of RA. Furthermore, the effective inhibition of prolactin secretion and/or action may have potential as therapy for RA.

Adult↗
PubMed1982

A possible direct effect of prolactin on follicular activity.

To examine whether high serum prolactin levels inhibit follicular maturation, prolactin was injected during diestrus of intact female rats or endogenous prolactin levels were raised by applying a suckling stimulus. Injections of rat prolactin (100 micrograms per injection) given 2 and 1 days before proestrus resulted in a lower estradiol production by proestrous follicles during a 4-h incubation period than follicles isolated from control rats. In 4 out of 7 animals this occurred without a change in serum progesterone and luteinizing hormone (LH) concentrations. In the 3 remaining animals corpus luteum function was activated. In these animals serum LH concentrations were decreased and follicular estradiol production was further suppressed. To study follicular development in the presence of suckling-induced hyperprolactinemia, the following experiment was performed. Removal of a 5-pup litter at Day 13 (0900 h) of lactation (Day 1 = day of parturition) resulted in ovulation at Day 16. Replacement of a new litter 24 h after litter removal did not interfere with ovulation on Day 16. This procedure allowed the study of follicular development between Days 14 and 15 in the presence of raised serum prolactin levels. It appeared that this treatment did not affect follicular growth, but in vitro estradiol production by preovulatory follicles isolated at Day 15 was lower than in follicles isolated from nonlactating animals. In 3 out of 13 animals corpus luteum function was reactivated. In these animals LH levels and follicular estradiol production were significantly suppressed. Treatment with bromocriptine (1 mg per injection) on Days 13 and 14, in addition to litter replacement, restored the high estradiol production at Day 15 without affecting serum LH concentrations. The results of this study demonstrate that in the presence of high prolactin levels, follicular estradiol production is low. The inverse relation between prolactin and follicular estradiol production in the presence of unchanged serum LH levels suggests that prolactin can have a direct action on estrogen biosynthesis of follicle cells.

Animals↗
PubMed1987

The roles of prolactin and testosterone in the development and function of granulosa lutein tissue in the rat.

The luteotropic roles of prolactin and testosterone (or estradiol formed in luteal tissue) were investigated in hypophysectomized rats with homografts of granulosa lutein tissue. Using this approach, we could determine the effects of prolactin independently of estrogen, since granulosa lutein tissue does not produce estrogen de novo under these conditions. Luteinizing granulosa cells were expressed from the ovaries of immature pregnant mare's serum gonadotropin-primed Fischer 344 rats 6 h after injection of human chorionic gonadotropin. The cells were transplanted beneath the kidney capsule of adult, hypophysectomized, ovariectomized Fischer 344 recipients, which were treated with hormones daily for 12 or 14 days. In rats without treatment (no hormones, n = 3) and in rats treated with only testosterone (Silastic capsule, n = 6), only small amounts of luteal tissue (less than 5 mg/rat) were found and serum progesterone remained at low concentrations (10 ng or less) throughout the experiment. In contrast, in rats treated either with ovine prolactin (300 micrograms/day, n = 10) or with the combination of prolactin and testosterone (n = 12), serum progesterone increased to 43 ng/ml by Day 8. Beyond Day 8, serum progesterone continued to rise in rats treated with the combination of prolactin and testosterone to reach a mean value of 87 ng/ml by Day 14, and mean homograft wet weight was 49 mg/rat; in rats treated with only prolactin, serum progesterone decreased to 25 ng/ml by Day 14 and homograft wet weight was lower (24 mg/rat). Prolactin and testosterone together stimulated more homograft aromatase activity in vivo than did prolactin alone, but the in vitro production of progesterone was not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cloning of decidual prolactin from rhesus macaque.

Rhesus monkey (Macaca mulatta) decidual prolactin cDNA was cloned and sequenced. The first 210 bp of the monkey sequence is not contiguous to the human pituitary prolactin transcription initiation site. Reverse transcription-polymerase chain reaction (RT-PCR) and Southern analysis confirmed that this 5'-extended prolactin transcript is present in monkey decidua but not in pituitary. Isolation and sequencing of a partial genomic monkey prolactin clone verified the nucleotide changes found in the rhesus cDNA. Comparison of the rhesus decidual prolactin cDNA to the human pituitary cDNA revealed more than 97% homology between the two. These data indicate that monkey prolactin mRNA from the decidualized endometrium of pregnancy contains unique 5' sequence not present in pituitary prolactin mRNA, suggesting the use of an alternative start site. Thus it is likely that the decidua uses promoter and regulatory regions different from those reported for pituitary prolactin.

Animals↗
PubMed1999

Seasonal variation in long-day stimulation of prolactin secretion in ewes.

Whereas ewes initiate reproductive activity in response to a photoperiod signal initiated after the winter solstice of 35 long days (35 LD) followed by short days, the reproductive axis fails to respond to this signal between the autumn equinox and the winter solstice. The aim of experiment 1 was to determine whether the prolactin axis, like the reproductive axis, is unresponsive to a 35 LD photoperiod signal followed by continuous exposure to short days between the autumn equinox and the winter solstice. Whereas the 35 LD signal from September 21 (</= 6 h increase in day length) failed to influence prolactin secretion, all other long-day treatments (> 6 h increase in day length) initiated a rise in prolactin in at least 75% of ewes in each group (p < 0.05). The aim of experiment 2 was to determine whether ewes failed to secrete prolactin during a 35 LD photoperiod from September 21 because they did not recognize a 6-h increase in day length at any time of year as a stimulatory photoperiod signal or because hypothalamic/pituitary regulation of prolactin synthesis or secretion is compromised in September. The results demonstrated that while hypothalamic regulation of prolactin secretion and pituitary stores of prolactin were normal at all times of year examined, the ability of ewes to secrete prolactin in response to a long-day photoperiod signal appears to be dependent on photoperiodic history rather than the time of year of the photoperiodic challenge.

Animals↗
PubMed1997

Androgen-dependent expression of prolactin in rat prostate epithelium in vivo and in organ culture.

Peptide hormones and growth factors are involved in the regulation of prostatic cell proliferation, differentiation, and programmed cell death, which functions are primarily controlled by androgen. In carcinogenesis, prostatic cancer cells often lose androgen dependence and become largely dependent on local growth factors. The prostatic cancer cells able to respond to factors other than androgen by proliferation and inhibition of apoptosis are possibly able to survive. We demonstrate that prostatic epithelium expresses prolactin mRNA and protein in a characteristic manner. By using in situ hybridization, an overall distribution of prolactin mRNA was demonstrated in the epithelium of rat dorsal and lateral prostate, whereas a very specific localization of prolactin protein to single cells was observed by immunohistochemistry in the same tissues. In these cells, immunoelectron microscopy showed that prolactin was primarily localized to the secretory granules. These data demonstrate a selective regulation of prostatic prolactin at least at the level of transcript processing/translation and/or protein accumulation and secretion. In addition, the expression of prolactin protein in rat dorsal and lateral prostate was found to be androgen dependent in vivo in castrated and in castrated, testosterone-treated rats, as well as in vitro in organ cultures. Our results support the concept of an autocrine/paracrine loop of prolactin action in prostate where it could mediate some of androgen actions. Also, locally synthesized prolactin might belong to the factors that take over androgen regulation of prostatic cancer cells during the development of androgen-independent growth.

Androgens↗
PubMed1986

Cysteamine decreases prolactin responsiveness to thyrotropin-releasing hormone in normal men.

Cysteamine depletes pituitary and plasma prolactin in rats. It acts through a nondopaminergic mechanism to alter both immunoactive and bioactive prolactin. The effect of cysteamine on prolactin secretion is reported in normal men. Six normal subjects received a control thyrotropin-releasing hormone (TRH) test at 0900 using 200 micrograms TRH intravenously; serum prolactin and TSH were measured at -10, 0, 10, 20, 30, 60, and 90 min after administration of TRH. Serum calcium and parathyroid hormones levels were measured at -10 min. Seven or more days later, they received cysteamine hydrochloride 15 mg/kg body weight orally every 6 hours for 5 doses. One hour after the last dose, the TRH test was repeated. Peak serum prolactin levels following TRH, prolactin levels at the 10-min time point, and total area from 0 to 30 min under the prolactin secretory curve were significantly decreased by cysteamine administration. TSH levels were unchanged. Serum calcium levels were significantly decreased by cysteamine administration, but parathyroid hormone levels were unchanged. It was concluded that cysteamine reduced TRH-stimulated prolactin secretion. Cysteamine also decreases serum calcium levels and suppresses the anticipated rise in serum parathyroid hormone levels. These effects on serum calcium and parathyroid hormone are similar to those previously shown for WR2721, another sulfhydryl compound. Cysteamine should be further considered as an alternative drug in the treatment of hyperprolactinemia and as a therapeutic agent for hypercalcemia.

Adult↗