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PubMedDate not supplied

Effect of the association time of in vivo bound prolactin on the [125I]prolactin receptor assays of female rat livers.

Significantly (P less than 0.01) reduced 125I-labeled ovine prolactin binding (mean, --22%), as a result of an ether anesthesia-reduced rise in serum prolactin, was observed in plasma membrane preparations of liver samples of female rats taken after 5 min of etherization when compared to samples taken from the same animals during the first minute of etherization. This reduction in assayable receptors occurred after 1 h but not 2 h of assay incubation time. Significantly (P less than 0.05) reduced 125I-labeled ovine prolactin binding (mean, --16%) was also observed in liver samples exposed to a 30-min ether-induced rise in serum prolactin when compared to liver samples taken during the first minute of etherization. In contrast, this reduction was apparent at assay incubation times of 1, 2 and 4 h but not at 10 h. These results suggest that serum prolactin can bind to prolactin receptors in vivo and partially block subsequent 125I-labeled ovine prolactin receptor assay. In addition, these data provide evidence that a complex time-dependent binding of prolactin may occur in the plasma of the female rat liver.

Animals↗

PubMed1997

Effects of bromocriptine on serum prolactin levels, pituitary weight and immunoreactive prolactin cells in estradiol-treated ovariectomized rats: an experimental model of estrogen-dependent hyperprolactinemia.

The present study was designed to assess the effects of bromocriptine, a dopamine agonist, on pituitary wet weight, number of immunoreactive prolactin cells and serum prolactin concentrations in estradiol-treated rats. Ovariectomized Wistar rats were injected subcutaneously with sunflower oil vehicle or estradiol valerate (50 or 300 micrograms/rat(-1) week (-1) for 2, 4, or 10 weeks. Bromocriptine (0.2 or 0.6 mg rat (-1) day (-1)) was injected daily during the last 5 or 12 days of estrogen treatment. Data were compared with those obtained for intact control rats. Administration of both doses of estrogen increased serum prolactin levels. No difference in the number of prolactin cells in rats treated with 50 micrograms estradiol valerate was observed compared to intact adult animals. In contrast, rats treated with 300 micrograms estradiol valerate showed a significant increase in the number of prolactin cells (P < 0.05). Therefore, the increase inn serum prolactin levels observed in rats treated with 50 micrograms estradiol valerate, in the absence of morphological changes in the pituitary cells, suggests a "functional" estrogen-induced hyperprolactinemia. Bromocriptine decreased prolactin levels in all estrogen-treated rats. The administration of this drug to rats previously treated with 300 micrograms estradiol valerate also resulted in a significant decrease in pituitary weight and number of prolactin cells when compared to the group treated with estradiol alone. The general antiprolactinemic and antiproliferative pituitary effects of bromocriptine treatment reported here validate the experimental model of estrogen-induced hyperprolactinemic rats.

Animals↗

PubMed1980

Tamoxifen suppresses both the growth of prolactin-secreting pituitary tumours and normal prolactin synthesis in the rat.

The effect of administering the antioestrogenic drug, tamoxifen, on the growth of the pituitary tumour 7315a in the rat was studied. This tumour is induced by the administration of oestrogen. When administered early after the implantation of the tumour, tamoxifen prevented its growth completely but when treatment was delayed until a later stage of its development, 20 microgram tamoxifen/100 g body wt each day for 7-12 days stopped further tumour growth, while 200 microgram/100 g body wt each day reduced the size of the tumours. These effects of tamoxifen on tumour growth were accompanied by a decrease in the level of prolactin in the circulation, if the treatment was started at an early stage of tumour development and if the high dose of tamoxifen was administered. Bromocriptine either when given alone or together with tamoxifen was unable to inhibit growth and secretion of prolactin by these rat pituitary tumours. The high plasma concentrations of prolactin in the tumour-bearing rats are known to produce atrophy of the pituitary gland of the host and to decrease the synthesis and release of prolactin. Despite the inhibitory effect of tamoxifen on both tumour size and plasma levels of prolactin, the ability of the pituitary glands of these animals to synthesize prolactin remained suppressed. It was concluded that tamoxifen has a dual effect on this model of a transplantable pituitary tumour that secretes prolactin in the rat; it prevents and/or inhibits tumour growth and it has an inhibitory effect on the synthesis of prolactin by the pituitary gland.

Animals↗

PubMed1992

An element in the prolactin promoter mediates the stimulatory effect of insulin on transcription of the prolactin gene.

An insulin response element (IRE) has been identified in the prolactin gene using chimeric plasmids in which prolactin promoter DNA directs expression of the bacterial chloramphenicol acetyltransferase gene. A series of 5'-deletion constructs starting between positions -173 and -106 and extending through position +75 of the prolactin gene were all stimulated greater than 10-fold by physiological concentrations of insulin in rat pituitary tumor GH4 cells. However, insulin did not stimulate constructs starting at positions -96 and -46, suggesting that the IRE of the prolactin gene may be located in region -106/-96. Insulin stimulation of prolactin-chloramphenicol acetyltransferase constructs requires cotransfection with a human insulin receptor expression vector. Estimation of insulin receptor levels by beta-subunit phosphorylation indicates that receptor levels are increased approximately 50-fold following transfection with the human insulin receptor expression vector. This requirement for cotransfection suggests that the endogenous receptor levels may not be adequate to couple the response of transfected genes to insulin. Gel mobility shift experiments reveal a nuclear factor from GH4 cells that specifically associates with prolactin DNA fragment -106/-87. The amount or binding activity of this factor is increased following insulin treatment of cells. The concordance between functional and binding analyses of the prolactin promoter confirms the presence of an IRE in region -106/-87. The insulin-sensitive DNA-binding factor may mediate effects of insulin on prolactin gene transcription.

Animals↗

PubMed1985

[Correlation of prolactin-secreting-capacity to circadian profile of prolactin in euprolactinemic women with ovulatory disturbances].

Circadian profile and responsiveness of prolactin to TRH administration were examined in 21 women with ovulatory disturbances. The data were analyzed with reference to the clinical effectiveness of bromocriptine administration. Resting levels of serum prolactin in the patients studied were lower than 25 ng/ml. 14 patients out of 16 cases (Group A) responded to bromocriptine, whose prolactin levels were more than 30 ng/ml during the night in the circadian studies. On the other hand, none of 5 patient (group B) responded to bromocriptine, whose prolactin levels were not more than 30 ng/ml during the night. Group A showed hyper-responsiveness of prolactin to TRH higher than that of Group B. These results suggested that 1) In euprolactinemic ovulatory disturbances there are cases with nocturnal hyperprolactinemia, whose prolactin levels are normal during the day time. These cases will be referred to as occult hyperprolactinemia. 2) Those with occult hyperprolactinemia show increased prolactin-secreting-capacity, which is able to be diagnosed by the hyper-responsiveness of prolactin to TRH administration. 3) The effectiveness of bromocriptine in treating euprolactinemic ovulatory disturbances is due to the suppressive effect of bromocriptine on the hyperprolactinemic states of occult hyperprolactinemia.

Adult↗

PubMed1986

Changes in serum prolactin concentrations and ovarian prolactin receptors during embryonic diapause in mink.

Experiments were conducted to determine if prolactin receptors were present in the mink ovary, and to examine the relationship between receptor numbers and serum levels of prolactin (PRL) during embryonic diapause and blastocyst reactivation. For analysis of the physicochemical properties of prolactin receptors, ovaries were obtained from anestrous mink. All binding determinations were made using 125I-ovine prolactin (125I-oPRL), and 20 micrograms of tissue protein from the 100,000 X g particulate fraction. To quantify prolactin receptors during gestation, 20 primiparous mink were mated twice on consecutive days between 4 and 10 March and assigned randomly to one of two groups. Mink in Group 1 (N=8) were killed on 13 March when blastocysts were completing their migration into the uterus and entering a state of diapause. Animals in Group 2 (N=10) were killed on 26 March during the period of blastocyst reactivation, just prior to implantation. To determine serum levels of prolactin during gestation, an additional 20 primiparous mink were similarly mated and bled every 4 days from 15 March to 8 April, and then every 7 days until 23 April. Prolactin concentrations were determined by a heterologous double antibody radioimmunoassay using porcine PRL for both tracer and standards. Optimum conditions for binding 125I-oPRL to ovarian membranes were attained at 25 degrees C after 12 h. Scatchard analysis revealed a single class of high affinity binding sites with a Kd of 6.14 X 10(-11) M. The total concentration of receptors during anestrus was 85 fmol/mg protein, which increased significantly during embryonic diapause to 484 fmol/mg protein, then declined to 16 fmol/mg during blastocyst reactivation.

Animals↗

PubMed2005

Stimulation and inhibition of prolactin release by prolactin-releasing Peptide in rat anterior pituitary cell aggregates.

Although the G-protein coupled receptor GPR10 is highly expressed in the anterior pituitary, the action of its ligand prolactin-releasing peptide-31 (PrRP) in this tissue is controversial. The present study examined the acute effect of this peptide on prolactin secretion in perifused rat pituitary reaggregate cell cultures from adult male rats. PrRP readily and dose-dependently stimulated prolactin release at concentrations of 10 and 100 nM, although with a magnitude several times lower than that of thyrotropin-releasing hormone. Surprisingly, PrRP inhibited prolactin release at 0.1 and 1 nm in a pertussis toxin-sensitive manner. Inhibition was markedly favoured by long-term culture. Stimulation and inhibition were differentially affected by the presence of hormones during culture: dexamethasone favoured the inhibitory effect and decreased the magnitude of the stimulatory effect, while oestradiol and triiodothyronine strongly reduced stimulation, as well as inhibition. PrRP, even at 1 nm, counteracted the inhibition of prolactin release by dopamine. There was no effect of PrRP on growth hormone release in aggregates cultured either in the absence or presence of hormones. The present results confirm the prolactin-releasing capacity of PrRP at nanomolar doses and reveal a hitherto unrecognized inhibitory activity of this peptide. Furthermore, dopamine inhibition of prolactin release is antagonized by PrRP, irrespective of the PrRP dose.

Animals↗

PubMed2006

Expression of the long form of the prolactin receptor in magnocellular oxytocin neurons is associated with specific prolactin regulation of oxytocin neurons.

Magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) show considerable plasticity during pregnancy and lactation. Prolactin receptors (PRL-R) have been identified in both these nuclei. The aim of this study was to investigate the cell type(s) expressing mRNA for the long form of prolactin receptor (PRL-R(L)) and to determine whether patterns of expression change during pregnancy and lactation. In addition, we examined effects of prolactin on excitability of oxytocin and vasopressin neurons. Sections from brains of nonpregnant, pregnant, and lactating rats were hybridized with an 35S-labeled probe to label PRL-R(L) mRNA together with digoxigenin-labeled probes to detect either oxytocin or vasopressin mRNA. In the SON, PRL-R(L) mRNA was predominantly colocalized with oxytocin mRNA, with over 80% of oxytocin neurons positive for PRL-R(L) mRNA. Very few (<10%) vasopressin neurons expressed PRL-R(L) mRNA. In the PVN, PRL-R(L) mRNA was also predominantly found in oxytocin neurons, and the proportion of PRL-R(L)-positive oxytocin neurons increased significantly during pregnancy and lactation. As in the SON, relatively few vasopressin cells contained PRL-R(L) mRNA. For in vivo electrophysiology, nonpregnant rats were anesthetized, and then extracellular single neuron activity was recorded in identified oxytocin and vasopressin neurons. After a period of baseline recording, the effect of prolactin (1 microg i.c.v.) on firing rate was examined. Prolactin treatment of nonpregnant rats induced a significant decrease in firing rates of oxytocin neurons. There was no effect of prolactin on the activity of vasopressin neurons. Together, these data provide strong evidence that prolactin directly and specifically regulates activity of oxytocin neurons.

Animals↗

PubMed1999

In vitro expression of long and short ovine prolactin receptors: activation of Jak2/STAT5 pathway is not sufficient to account for prolactin signal transduction to the ovine beta-lactoglobulin gene promoter.

The recent finding that sheep had long (l-oPRLR) and short (s-oPRLR) prolactin receptors provided new tools to further explore prolactin signaling to target genes. Here we used CHO cells transfected with l-oPRLR or s-oPRLR cDNAs to compare the activation of known key steps of prolactin signaling by the two receptors. We found that prolactin stimulated l-oPRLR tyrosine phosphorylation, although it lacked the last tyrosine residue found in other long prolactin receptors. In addition, l-oPRLR and s-oPRLR both responded to prolactin stimulation by (1) Janus kinase 2 (Jak2) tyrosine phosphorylation, (2) DNA-binding activation of signal transducer and activator of transcription 5 (STAT5), (3) stimulation of transcription from a promoter made of six repeats of STAT5-responsive sequence. However, although it contains STAT5-binding consensus sequences, the ovine beta-lactoglobulin promoter (-4000 to +40) was transactivated by l-oPRLR, but not by s-oPRLR. Taken together, our results indicate that activation of Jak2/STAT5 pathway alone is not sufficient to account for prolactin-induced transcription of this milk protein gene, and that sequences of its promoter, other than STAT5-specific sequences, account for the opposite transcriptional activation capabilities of l-oPRLR and s-oPRLR.

Animals↗

PubMed2003

Prolactin release during the estradiol-induced LH surge in ewes: modulation by progesterone but no evidence for prolactin-releasing peptide involvement.

An estradiol-induced prolactin surge accompanies the LH surge in several species, including sheep. However, the neural mechanisms underlying this surge remain poorly understood. A first study on estradiol- and progesterone-treated ovariectomized ewes examined whether the prolactin surge, like the LH surge, is sensitive to progesterone. Our data clearly showed that the estradiol-induced prolactin surge in the ewe is blocked by continuous exposure to progesterone and, importantly, that this blockade is overcome by pretreatment with the progesterone receptor antagonist, RU486. In a second study, we established that the generation of the prolactin surge is not dependent on the co-secretion of a prolactin-releasing peptide in the hypophyseal portal blood or cerebrospinal fluid. The neuronal pathways targeted by estradiol and progesterone to modulate prolactin secretion at the time of the LH surge remain to be identified. Importantly, it has not been established whether there is any overlap in the neuronal systems generating the gonadotropin-releasing hormone and prolactin surges.

Animals↗

PubMed2001

Anxiolytic and anti-stress effects of brain prolactin: improved efficacy of antisense targeting of the prolactin receptor by molecular modeling.

We provide the first evidence that prolactin is a neuromodulator of behavioral and neuroendocrine stress coping in the rat. In virgin female and male rats, intracerebral infusion of ovine prolactin (oPRL) into the lateral cerebral ventricle (intracerebroventricular) exerted an anxiolytic effect on the elevated plus-maze in a dose-dependent manner (0.1 and 1.0 microg/5 microl; p < 0.01). In contrast, downregulation of the expression of the long form of brain prolactin receptors by chronic intracerebroventricular infusion of an antisense oligodeoxynucleotide (ODN) (osmotic minipump, 0.5 microg. 0.5 microl(-1). hr(-1); 5 d) increased anxiety-related behavior on the plus-maze compared with mixed bases-treated and vehicle-treated rats (p < 0.01), again demonstrating an anxiolytic effect of PRL acting at brain level. Furthermore, in jugular vein-catheterized female rats, the stress-induced increase of corticotropin secretion was decreased after chronic intracerebroventricular infusion of oPRL (osmotic minipump, 1.0 microg. 0.5 microl(-1). hr(-1); p < 0.05) and, in contrast, was further elevated by antisense targeting of the brain prolactin receptors (p < 0.01). This provides evidence for a receptor-mediated attenuation of the responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis by prolactin. The antisense ODN sequence was selected on the basis of secondary structure molecular modeling of the target mRNA to improve antisense ODN-mRNA hybridization. Receptor autoradiography confirmed the expected improvement in the efficacy of downregulation of prolactin receptor expression [empirically designed antisense, 30%; p > 0.05, not significant; adjustment of target position after mRNA modeling, 72%; p < 0.05). Taken together, prolactin acting at brain level has to be considered as a novel regulator of both emotionality and HPA axis reactivity.

Adrenocorticotropic Hormone↗

PubMed1989

Mechanisms that subserve estradiol's induction of increased prolactin concentrations: evidence of amplitude modulation of spontaneous prolactin secretory bursts.

Estradiol stimulates hyperprolactinemia in human beings and in experimental animals by mechanism(s) that remain largely undefined. We have tested the hypothesis that estrogen modulates episodic and rhythmic prolactin release. To this end we studied six postmenopausal women by repetitive venous sampling basally and on days 1, 5, 10, and 30 after intravaginal placement of an estradiol-impregnated polymeric silicone (Silastic) ring. Computerized analysis of episodic prolactin pulsatility revealed that estrogen amplified prolactin pulse amplitude threefold without changing prolactin pulse frequency. Fourier analysis disclosed heightened amplitudes of specific ultradian rhythms, and deconvolution analysis demonstrated a sevenfold increase in the mass of prolactin secreted per pulse with no change in its half-life. We conclude that estradiol selectively augments the amplitude of episodic prolactin pulsatility, amplifies ultradian rhythms, and increases the mass of prolactin released per secretory burst.

Activity Cycles↗

PubMed1976

Effects of intraventricular 6-hydroxydopamine injections on serum prolactin and LH levels: absence of stress-induced pituitary prolactin release.

The drug 6-hydroxydopamine (6-OHDA) has been reported to reduce hypothalamic norepinephrine (NE) content after administration into the lateral ventricle without altering the dopamine content of tubero-infundibular neurons. Serum prolactin levels in male rats injected with 2 X 250 mug 6-OHDA were significantly higher than in untreated control rats. Intraventricular injection of male rats with artificial cerebrospinal fluid resulted in elevated mean prolactin levels similar to those observed in 6-OHDA-treated animals. Further experimentation on animals decapitated at different times after removal from the animal quarters, indicates that prolcatin levels in 6-OHDA-treated rats are continuously elevated whereas they rise from basal levels to extremely high levels in CSF-treated rats, thus resulting in similar mean values. The CSF-treated controls ate hypersensitive to the stress of being removed from their normal environment. Such an effect was not observed in 6-OHDA-treated nor in untreated, and thus stress-inexperienced rats. In a long term study, serum prolactin and luteinizing hormone (LH) levels were followed over a period of 71 days after 6-OHDA treatment. Prolactin levels increased within one day after treatment and stayed at a high level for 15 days. Subnormal prolactin values were measured 37 days after 6-OHDA treatment. Serum LH levels were below normal 3 h and one day and were increased 37 and 71 days after 6-OHDA treatment. These results suggest that NE is important in the transmission of stressful stimuli to hypothalamic prolactin regulating centers. They further suggest functional recovery of LH and prolactin regulating mechanisms after 6-OHDA treatment.

Animals↗

PubMed1989

New aspects of prolactin and immunity: a lymphocyte-derived prolactin-like product and nuclear protein kinase C activation.

In addition to its growth regulating properties, new evidence reviewed here by Diane Haddock Russell demonstrates that prolactin has important immunoregulatory properties. In immune-compromised dwarf mice, prolactin restores immunocompetence. Human lymphocytes have prolactin receptors and mitogen-stimulated lymphocytes make and secrete a prolactin-like activity. Prolactin can stimulate the activation of nuclear protein kinase C in spleen and liver isolated nuclear preparations. This activation is blocked by prolactin receptor monoclonal antibody, suggesting that there is a receptor-mediated activation process in the nucleus. The discovery of the ability of prolactin and growth factors to activate nuclear protein kinase C may constitute a breakthrough in our understanding of how these hormones regulate trophic responses.

Cell Nucleus↗

PubMed2004

Changes of prolactin regulatory mechanisms in aging: 24-h rhythms of serum prolactin and median eminence and adenohypophysial concentration of dopamine, serotonin, (gamma-aminobutyric acid, taurine and somatostatin in young and aged rats.

Twenty-four hour rhythmicity of serum prolactin and median eminence and anterior pituitary content of dopamine (DA), serotonin (5HT), gamma-aminobutyric acid (GABA), taurine and somatostatin were examined in 2 months-old and 18-20 months-old Wistar male rats. The concentration of prolactin was higher in aged rats, with peaks in both groups of rats at the early phase of the activity span. Median eminence DA content of young rats attained its maximum at the middle of rest span and decreased as prolactin levels augmented while the lowest values of adenohypophysial DA were observed at the time of prolactin peak. DA rhythmicity disappeared in aged rats. GABA content of median eminence and adenohypophysis was lower in aged rats, with maximal values of median eminence GABA at light-dark transition in young rats and at the second half of activity span in aged rats. Serum prolactin correlated positively with median eminence GABA in young rats and negatively with pituitary GABA in young and aged rats. Median eminence somatostatin peaked at the beginning of the activity phase (young rats) or at the end of the rest phase (aged rats). Prolactin levels and somatostatin content correlated significantly in young rats only. Median eminence and pituitary 5HT and taurine content did not change with age. The results indicate disruption of prolactin regulatory mechanisms with aging in rats.

Aging↗

PubMed1979

Prolactin-secreting pituitary adenomas in women. II. Menstrual function, pituitary reserves, and prolactin production following microsurgical removal.

A prospective study of 46 women with prolactin-secreting pituitary adenomas and amenorrhea and/or galactorrhea was performed to determine the influence of the selective transsphenoidal removal of these tumors on pituitary and reproductive function. This procedure was effective in restoring menstrual function in 34 of 41 women and in eliminating lactation in 30 of 40 women. Tumor size and preoperative serum prolactin concentrations were the most important factors in predicting the postoperative disappearance of symptoms. Normal menstrual function returned in 33 of 34 women with tumors less than 2 cm in diameter but in only one of seven women with tumors greater than 2 cm. Similarly, galactorrhea disappeared in 29 of 34 women with tumors less than 2 cm but in only one of six women with larger tumors. Menses returned in 31 of 32 women and galactorrhea disappeared in 25 of 31 women with preoperative serum prolactin levels below 200 ng/ml; conversely, menses returned in only three of nine women and lactation ceased in one of six women with preoperative serum prolactin concentrations above 200 ng/ml. Prolactin concentrations decreased in 42 of 43 patients following the removal of pituitary adenomas and returned to normal in 30. Postoperative pituitary reserves of adrenocorticotropic hormone, growth hormone, luteinizing hormone, and follicle-stimulating hormone were normal in most patients. These data indicate that the removal of prolactin-secreting pituitary adenomas by a neurosurgeon accomplished in this surgical technique is effective in restoring menstrual function and eliminating lactation in most women, especially if the tumor is less than 2 cm in diameter and the preoperative serum prolactin concentration is less than 200 ng/ml.

Adenoma↗

PubMed1999

Retinoic acid modulates prolactin receptor expression and prolactin-induced STAT-5 activation in breast cancer cells in vitro.

Two recent papers demonstrate that prolactin plays an important role in the induction and progression of mammary tumours. Retinoids have been shown to be potent inhibitors of breast carcinogenesis. We studied expression of prolactin receptor mRNA in human breast cancer cell lines MCF-7, SKBR-3, T47D and BT-20 treated with and without retinoids using Northern blot and a quantitative polymerase chain reaction (PCR) method. In all cell lines, all-trans- and 9-cis-retinoic acid, as well as the retinoic acid receptor gamma (RAR-gamma) selective agonists CD2325 and CD437 (1 microM), were able to down-regulate prolactin receptor. After 1 h, a significant reduction was detectable and maximal effect was achieved after 24 h of treatment. Pretreatment with retinoic acid also reduced the prolactin-/prolactin receptor-dependent signal transduction and activation of transcription 5 (STAT-5) activation in T47D cells. Cycloheximide failed to abrogate the retinoic acid-induced decline in prolactin receptor mRNA levels, indicating that this effect was not dependent upon continuing protein synthesis. Similarly, no change in the stability of prolactin receptor mRNA was observed during 12 h of retinoic acid treatment. In conclusion, our results demonstrate that retinoids are able to inhibit the expression of prolactin receptor message, which encodes an important growth factor receptor in breast cancer cells. This action could be responsible for the anti-tumour effects of retinoids.

Alitretinoin↗

PubMed2001

Polymorphisms of the human prolactin gene--implications for production of lymphocyte prolactin and systemic lupus erythematosus.

Hyperprolactinaemia is associated with systemic lupus erythematosus (SLE) but the mechanism is unknown. Prolactin is expressed not only by pituitary lactotrophic cells but also by T-lymphocytes under the control of an alternative upstream promoter region. T-lymphocytes from SLE patients have been shown to secrete more prolactin than controls, thus implying a possible underlying difference in regulation. This may be due to genetic polymorphism that can be determined by scanning for mutations and using a variety of methods to determine their function. A polymorphism may also be used in disease association studies as it may be in linkage disequilibrium with a disease gene on the same haplotype. Single nucleotide polymorphisms (SNPs) have been found across the prolactin gene region including the extrapituitary and the pituitary promoter regions. These SNPs have been examined for genetic association with SLE and potential effects upon the function of the gene. One SNP in the lymphocyte specific upstream promoter affects prolactin transcription and disease association studies in a cohort of SLE cases demonstrated an increased frequency of the PRL-1149 G allele compared to control subjects. This indicates a possible mechanism for the association of prolactin with SLE. Although prolactin is likely to be one of several predisposing factors in the pathogenesis and progression of SLE, this suggests that manipulation of lymphocyte prolactin production (rather than pituitary production) might be a useful therapeutic approach.

Gene Expression Regulation↗