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At least 883 records · Page 49Linked to original sources
PubMed1985

Modulation of prolactin binding sites in vitro by membrane fluidizers. Effects on male prostatic and female hepatic membranes in alcohol-fed rats.

The objectives of this study were (i) to determine if in vivo administration of ethanol to rats produced changes in apparent lipid fluidity and prolactin binding capacity of male prostatic and female hepatic membranes and (ii) to compare the effects of membrane fluidizers (aliphatic alcohols) in vitro on prolactin binding of prostatic and hepatic membranes in control and alcohol-fed animals. In vitro ethanol has been shown by us previously to increase prolactin receptor levels presumably by unmasking cryptic prolactin receptors. The degree of fluidization was monitored by a fluorescence polarization method using 1,6-diphenylhexatriene. Adult male and female rats were given either water or 4% ethanol as the sole source of drinking fluid for a period of 6 weeks. No significant changes in plasma prolactin were observed between control and ethanol-treated groups of either sex. However, the microviscosity parameter, inversely related to lipid fluidity, was increased approx. 34% and 40%, respectively, in male prostatic and female rat hepatic membranes after ethanol feeding. Furthermore, 125I-prolactin binding capacity was decreased approx. 30% and 26%, respectively, in prostatic and hepatic membranes of alcohol fed animals. In vitro treatment with aliphatic alcohols had no effect on either microviscosity or prolactin binding in hepatic or prostatic membranes from ethanol-fed rats, but both fluidized and increased prolactin binding in the same membrane preparations from control rats. Our observations are consistent with the direct relationship between membrane fluidity and prolactin receptor levels. The changes in prostatic and hepatic membranes after alcohol feeding, namely decreased prolactin receptor levels, decreased fluidity and increased resistance to the fluidizing effects of in vitro aliphatic alcohols may reflect a fundamental membrane defect.

1-Butanol↗
PubMed1999

Prolactin receptor localization to the area postrema.

The area postrema, which lacks a blood-brain barrier, was examined for the presence of prolactin receptors, which would render it a potential site for vascular prolactin to directly interact with neuronal elements. Using an in vitro autoradiographic technique, frozen sections of New Zealand white rabbit medulla were incubated with radiolabelled ovine prolactin alone (total binding) or radiolabelled ovine prolactin in the presence of excess unlabelled ovine prolactin (non-specific binding). The specificity of the binding was also assessed using excess unlabelled human prolactin or ovine LH. While excess unlabelled ovine and human prolactin caused a statistically significant reduction in radio labeled prolactin binding, unlabelled LH was without effect. Results reveal the presence of specific prolactin binding sites within the area postrema, a previously unknown prolactin target area of the CNS.

Animals↗
PubMed1999

The prolactin receptor from the brushtail possum (Trichosurus vulpecula): cDNA cloning, expression and functional analysis.

A full length, prolactin receptor cDNA clone has been isolated from the brushtail possum (Trichosurus vulpecula). This clone encodes a 625 amino acid protein which shares 60-70 and 54% sequence identity with prolactin receptor (long form) sequences from mammalian and avian species, respectively. Sequence similarity was highest in the extra-cellular, hormone-binding domain and in specific regions of the intracellular domain which regulates prolactin receptor signalling in cells. Prolactin receptor mRNA was detected in a wide range of possum tissues and in the mammary gland the PRL-R gene was differentially expressed during lactation with peak mRNA levels being detected during the first 6 days of lactation and after day 115 throughout late lactation. This pattern of PRL-R mRNA expression in the mammary gland is similar to that observed for circulating prolactin in the lactating possum. In CHO cells transiently transfected with the possum prolactin receptor, expression of a beta-lactoglobulin promoter/reporter gene construct was increased 3-fold by adding prolactin. The possum prolactin receptor is therefore capable of binding ovine prolactin and activating the Jak2/Stat5 signalling cascade. This provides evidence for the highly conserved nature of the prolactin signalling pathway in mammalian evolution.

Amino Acid Sequence↗
PubMed1995

Regulation of pigeon cropmilk secretion and parental behaviors by prolactin.

Prolactin stimulates the growth and development of specialized epithelial cells lining the cropsac of pigeons and doves (family Columbidae), leading to formation of "cropmilk," which is fed to the newly hatched squab. This system of milk feeding is unique among birds. To support the feeding of cropmilk, a complex array of behavioral adaptations are also supported by high levels of prolactin secretion in columbids during parenting. These specializations include elevated food intake (hyperphagia), nest attendance, and regurgitation feeding of the squab. Although prolactin is clearly important for these behavioral adaptations, the precise physiological and mechanistic bases for these behavioral effects remain controversial. The molecular mechanisms of prolactin action in the cropsac epithelium have been studied by cloning prolactin-induced genes, by cloning and expressing the pigeon prolactin receptor, and by analyzing the transcription factors that are activated after prolactin treatment. The avian (pigeon) prolactin receptor is a member of the cytokine receptor superfamily and uniquely contains a complete duplication of the extracellular ligand-binding domain. One of the early signal-transducing actions of prolactin in cropsac epithelium is the activation of signal transducer and activator of transcription (STAT) proteins via tyrosine phosphorylation. This fundamental signaling pathway is shared with mammalian prolactin target tissues. The convergent evolution of milk feeding and the behaviors that support parenting in columbids and mammals has depended on adaptation of both conserved mechanisms and divergent physiological processes.

Animals↗
PubMed2005

Prolactin specifically activates signal transducer and activator of transcription 5b in neuroendocrine dopaminergic neurons.

The hypothalamic neuroendocrine dopaminergic (NEDA) neurons are crucial in regulating prolactin secretion from the anterior pituitary. Rising prolactin concentrations stimulate these neurons to secrete dopamine, which acts via the pituitary portal vasculature to inhibit additional prolactin release. Prolactin is known to activate Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathways in other cell types, including neurons. The possible role of JAK-STAT signaling in NEDA neurons has therefore been examined in this study using fetal rat mediobasal hypothalamic cell cultures and an adult rat in vivo preparation. Cultured cells expressing the dopamine synthesizing enzyme tyrosine hydroxylase (TH) responded to prolactin with a time-dependent increase in phospho-STAT5, but not phospho-STAT1 or phospho-STAT3, nuclear labeling. This response was inhibited by the prolactin receptor antagonist Delta1-9-G129R-human prolactin and the JAK inhibitor AG490, but was unaffected by selected serine/threonine kinase inhibitors (H89, KN-93, bisindolymaleimide, or PD98059). Antibodies selective for STAT5a or STAT5b indicated that the response was restricted to STAT5b, with the number of TH cells displaying STAT5b nuclear immunoreactivity rising from less than 10% under basal conditions to approximately 70% after prolactin stimulation. STAT5a nuclear labeling remained unchanged at 6-10% of TH-positive cells. STAT5b selectivity was confirmed in vivo, where the injection of prolactin into bromocriptine-treated rats stimulated a time-dependent increase in STAT5b, but not STAT5a, nuclear staining in the TH-expressing neurons in the arcuate nucleus. These results extend our previous findings with STAT5b-deficient mice and strongly suggest that in NEDA neurons, prolactin signaling via the JAK/STAT pathway is mediated exclusively by STAT5b.

Active Transport, Cell Nucleus↗
PubMed2006

Prolactin delays hair regrowth in mice.

Mammalian hair growth is cyclic, with hair-producing follicles alternating between active (anagen) and quiescent (telogen) phases. The timing of hair cycles is advanced in prolactin receptor (PRLR) knockout mice, suggesting that prolactin has a role in regulating follicle cycling. In this study, the relationship between profiles of circulating prolactin and the first post-natal hair growth cycle was examined in female Balb/c mice. Prolactin was found to increase at 3 weeks of age, prior to the onset of anagen 1 week later. Expression of PRLR mRNA in skin increased fourfold during early anagen. This was followed by upregulation of prolactin mRNA, also expressed in the skin. Pharmacological suppression of pituitary prolactin advanced dorsal hair growth by 3.5 days. Normal hair cycling was restored by replacement with exogenous prolactin for 3 days. Increasing the duration of prolactin treatment further retarded entry into anagen. However, prolactin treatments, which began after follicles had entered anagen at 26 days of age, did not alter the subsequent progression of the hair cycle. Skin from PRLR-deficient mice grafted onto endocrine-normal hosts underwent more rapid hair cycling than comparable wild-type grafts, with reduced duration of the telogen phase. These experiments demonstrate that prolactin regulates the timing of hair growth cycles in mice via a direct effect on the skin, rather than solely via the modulation of other endocrine factors.

Animals↗
PubMedDate not supplied

Endogenous prolactin maintains its own binding sites in the pigeon crop sac mucosa.

The specific binding of lactoperoxidase-labelled 125I-labelled ovine prolactin was determined in a membrane particulate of the pigeon crop-sac mucosal epithelium. Binding was found to be dependent upon the particulate preparation used, its protein concentration and the length of the incubation at 5 degrees C. Scatchard analysis of the binding to crop-sacs from saline or prolactin-injected (1.9 microgram per pigeon) revealed that prolactin stimulated 7-fold its own receptors by increasing the number of binding sites per mg protein: saline - 392 +/- 75 fmol/mg protein and prolactin 2736 +/- 602 fmol/mg protein (p less than 0.01). This increase did not affect the affinity constant (Ka): saline - 5.28 +/- 0.75 x 10(8) l/mol and prolactin 3.28 +/- 0.40 x 10(8) l/mol (N.S.), in keeping with the stimulatory effect of prolactin in the rat liver and mammary glands. This study further demonstrates the physiological role of endogenous prolactin in maintaining its own binding-sites in the pigeon crop-sac, since the administration of 0.8 ml anti-serum to prolactin resulted in a 63% reduction in the specific binding of labelled hormone in vitro. These results confirm the prolactin binding to the pigeon crop-sac mucosa, quantify the stimulation of this binding by prolactin itself, and demonstrate the role of the endogenous hormone in the maintenance of these receptors.

Animals↗
PubMed1988

Prolactin binding and localization in rat mammary tumor mast cells.

We found that prolactin is taken up by mast cells residing in prolactin-dependent, 7,12-dimethylbenzanthracene-induced rat mammary tumors. Light and electron microscopic immunocytochemistry showed that mast cells concentrate prolactin in their cytoplasmic granules. No prolactin was found on mast cell surface membranes or in their nuclei. In primary cultures of tumor cells, mast cells were found mainly in the periphery of dome structures and these cells concentrated prolactin. When purified rat peritoneal mast cells were incubated with 125I-labeled prolactin, uptake was time, energy, and temperature dependent. Seventy % of accumulated prolactin was released intact from cytoplasmic granules by C48/80-induced degranulation. A mouse mastocytoma cell line also took up and released prolactin. These cells contained prolactin receptors (Kd = 4.5 nM) as determined in whole cells (approximately 3150 sites/cell) and in crude membranes (approximately 180 fmol/mg protein). We conclude that mast cells might significantly influence mammary tumor growth by accumulating and releasing prolactin within tumor tissue.

Adenocarcinoma↗
PubMed1987

Role of serum in the prolactin responsiveness of MCF-7 human breast cancer cells in long-term tissue culture.

MCF-7 human breast cancer cells, grown in long-term tissue culture, were found to be highly responsive to prolactin in terms of growth even in the presence of serum. Human prolactin, placental lactogen, and growth hormone (50-250 ng/ml) stimulated MCF-7 cells to grow when added to culture medium of cells in the presence of charcoal-stripped serum. Within 3 days of the hormone addition, a 4.4-fold increase in cell number was achieved with human prolactin at 100 ng/ml in the presence of 10% charcoal-stripped serum. Under these same conditions, estradiol-17 beta at 10(-8) M achieved only a 2-fold increase. After 6 days of culture, both estradiol-17 beta and prolactin gave a total 5-fold increase in cell number. No prolactin effect was achieved in the presence of 10% fetal bovine serum. Stripping fetal bovine serum with dextran-coated charcoal removes as much as 85% of the endogenous lactogens. Removal of these hormones is essential for demonstration of subsequent prolactin-induced growth response in MCF-7 cells, since bovine prolactin binds effectively to lactogen receptors on the surface of the cells but does not transmit a growth signal. When added simultaneously with human prolactin, bovine prolactin blocks the growth response to the former hormone. These results clearly demonstrate that, under the proper conditions of culture, the human breast cancer cell line MCF-7 is highly responsive to growth stimulation by homologous lactogenic hormones. This then affords us an excellent model for further studies on the possible role of prolactin in growth and maintenance of human breast cancer.

Blood↗
PubMed1982

Prolactin and certain obstetric stress conditions.

Prolactin levels were evaluated during certain stress conditions, obstetric or gynecologic surgical interventions, labor, and birth. In 68 patients undergoing voluntary abortion, prolactin levels were measured to study the effect of anesthetics and of dilatation and curettage on hormonal secretion. Prolactin levels were evaluated in five patients undergoing elective cesarean section and in five post-menopausal patients undergoing total abdominal hysterectomy with bilateral oophorectomy. Moreover, prolactin concentration in serial samples of blood was estimated in 32 normal patients with spontaneous vaginal delivery at term and in 16 newborns at term after 30-60 and 120 min following birth. Prolactin responsiveness to TRH was evaluated in 12 newborns at the 4th day of life. Plasma prolactin levels rose in all the stress conditions investigated except in labor, during which hormone levels showed a decrease starting 2 h before delivery and reaching the lowest value 1 h prior. From this moment on there was a remarkable rise in prolactin concentration, with a peak 1 h after delivery. The decrease in prolactin levels during labor could possibly be due to an increase in dopaminergic activity. Moreover, the finding of no variation of prolactin levels during induced abortion in a group of patients pretreated with methysergide supports the view that the serotoninergic system also affects prolactin release.

Abortion, Induced↗
PubMed1975

[TRH stimulation as an attempt at demonstration of the induction and involution of prolactin-secreting pituitary cells in pregnancy and puerperium and in pathological hyperprolactinemia].

The present paper discusses the relationship between functional hypertrophia or hyperplasia of the prolactin secreting cells in the pituitary and actual pituitary prolactin reserves in pregnant and post partum women. 35 randomly selected post partum patients from the 3rd to 12th day p.p. and 14 women in their 11th to 14th weeks of pregnancy volunteered to undergo a standard TRH-test. The control group consisted of 60 normoprolactinemic patients. Eleven pathologically hyperprolactinemic patients were compared to the normoprolactinemic and physiologically hyperprolactinemic groups. In all cases, plasma prolactin showed a linear decrease from the 3rd to 12th days post partum. The TRH induced increase became correspondingly greater as the basal prolactin levels decreased, i.e. an inverse relationship between these two parameters was seen. The TRH-induced increase was also always greater than the increase caused by suckling. A connection between prolactin and parity was not found. The inverse relationship between basal prolactin levels and the actual reserves which could be released by TRH stimulation can be explained in that there are two regulatory systems for prolactin. The estrogens stimulate basal prolactin and inhibit prolactin reserves. The actual prolactin reserve is, on the one hand, directly dependent on the degree of endogenous neurohormonal stimulation and, on the other hand, indirectly dependent on the endogenous estrogens through a feedback mechanism. The TRH-stimulation test is not suitable for determining a functional hypertrophia or hyperplasia of lactotropic pituitary cells.

Estrogens↗
PubMed1994

Plasma prolactin in patients with colorectal cancer. Value in follow-up and as a prognosticator.

BACKGROUND: Preoperative plasma prolactin and carcinoembryonic antigen (CEA) levels were assessed to monitor disease recurrence and to identify low-risk and high-risk patients with Dukes B or C colorectal cancer. METHODS: Prolactin and CEA were estimated by radioimmunoassay method. Blood samples were collected preoperatively and sequentially thereafter from patients with colorectal cancer (N = 114); the samples were compared with samples from age-matched healthy control subjects (smokers and nonsmokers, N = 45). For rest of the analysis, patients with Dukes A disease (N = 7) were not included because of the small number. In monitoring recurrences, the criteria for positive test for the two markers was a continual increase in the marker level after an initial decrease or persistent high level of the marker. These were the indicators of relapse or no response to treatment. To determine the efficacy of the preoperative markers, the patients were grouped according to disease status at the end of 3 years, i.e., patients who had response to the treatment modalities (N = 52) and patients who later had progressive disease (N = 55). To determine the prognostic significance of preoperative marker levels, the patients were divided according to the cutoff levels (upper normal limits); for prolactin the cutoff level was 20.0 ng/ml plasma, and for CEA it was 5.0 ng/ml plasma. RESULTS: Both of the markers were significantly high in patients with colorectal cancer compared with the markers of their respective control subjects (P < 0.0001). In monitoring disease course, the predictive power of prolactin was 100%, whereas that of CEA was 66%. Prolactin showed a lead time of 2-3 months. Preoperative prolactin levels were significantly higher in patients who later had progressive disease (P < 0.001) than in patients who had response to the treatments. However, such an intergroup variation was not observed for CEA. Patients with preoperative levels of prolactin greater than 20.0 ng/ml had shorter overall survival times than did those with prolactin levels less than 20.0 ng/ml plasma; such a trend was not observed for patients with CEA levels less than 5.0 ng/ml and those with CEA levels greater than 5.0 ng/ml plasma. CONCLUSION: Prolactin is a better overall marker than is CEA in patients with Dukes B or C colorectal cancer. The authors recommend the use of plasma prolactin levels to help identify low-risk and high-risk patient subgroups so that high-risk patients may be followed up more intensely and treated accordingly. Hyperprolactinemic patients with Dukes B or C disease have shortened survival time.

Adult↗
PubMed2007

Reproductive factors and family history of breast cancer in relation to plasma prolactin levels in premenopausal and postmenopausal women.

Many reproductive factors are associated with breast cancer risk, potentially through a hormonal pathway. The peptide hormone prolactin is essential in mammary development and lactation and may be a link between risk factors and breast cancer. While higher prolactin levels are associated with increased breast cancer risk, few determinants of prolactin levels are known. We conducted a cross-sectional analysis among 1,089 premenopausal and 1,311 postmenopausal women within the Nurses' Health Study (NHS) and the NHS II to examine the associations of reproductive factors, benign breast disease and family history of breast cancer with plasma prolactin levels. Parous women had significantly lower prolactin levels than nulliparous women (parous vs. nulliparous multivariate-adjusted geometric means = 14.1 ng/mL vs. 16.6 ng/mL, p<0.001 for premenopausal and 9.1 vs. 10.1, p=0.04 for postmenopausal women), although levels did not decrease with increasing number of children for either premenopausal (p-trend = 0.23) or postmenopausal (p-trend = 0.07) parous women. Age at first birth was not associated with prolactin levels. The reduction in prolactin levels among parous premenopausal women appeared to attenuate with increasing time since first birth, but the trend was not statistically significant (p-trend = 0.12). Age at menarche, duration of lactation and benign breast disease were not associated with prolactin levels. Family history of breast cancer was associated with significantly higher prolactin levels when compared with no family history among premenopausal (15.9 ng/mL vs. 14.3 ng/mL, p=0.04) but not postmenopausal (p=0.73) women. In conclusion, the associations of parity and family history with breast cancer risk may be mediated, at least in part, by prolactin levels.

Adult↗
PubMed1984

Nyctohemeral changes in plasma prolactin levels and their relationship to breast cancer risk.

The amount of prolactin has been determined in serial blood samples taken over 24 h from 20 pre- and 9 postmenopausal women volunteers. All women had a large increase in prolactin at night (24.00 h-03.00 h). A much smaller rise in prolactin occurred in the evening (18.00 h-20.00 h) which was just significantly different (p less than 0.05) from levels found in the afternoon. Prolactin concentrations at any given time in the 29 women were linearly correlated with corresponding levels in either of the adjacent time intervals. This correlation was highly significant (p less than 0.001) throughout 24 h, implying that a woman with a relatively high (or low) blood prolactin in the afternoon would have a similarly high (or low) concentration in the evening or at night. Premenopausal women had higher amounts of prolactin than postmenopausal volunteers throughout the day. Parity was found to be inversely related to prolactin levels in pre- and postmenopausal women; this effect was especially marked in the night peak of prolactin. In postmenopausal women an average of 33 years had elapsed since the birth of the last child, which implies that childbirth has a life-long effect on reducing prolactin levels. Thus the protective effect of early child-bearing and multiparity against developing breast cancer could be at least partly explained by these effects on serum prolactin levels.

Breast Neoplasms↗
PubMed1982

Biochemical and immunohistochemical characterization of prolactin binding in rat ventral, lateral, and dorsal prostate lobes.

A radioligand assay and the soluble peroxidase-antiperoxidase (PAP) technique were used to compare ovine and rat prolactin as ligands for the demonstration of prolactin binding sites in rat ventral, lateral, and dorsal prostate lobes. Biochemical techniques were effective in demonstrating prolactin binding sites in ventral prostate with both ovine and rat prolactin; however, binding sites could not be characterized in lateral or dorsal lobes with either ligand. Using the PAP technique, rat prolactin consistently produced a discrete, dense reaction product over binding sites in the Golgi zone of the ventral prostate; ovine prolactin produced a more dispersed pattern of staining throughout the entire supranuclear region of the cells. In ventral prostate, most epithelial cells were immunoreactive when either ligand was used. However, lateral prostate contained fewer densely immunoreactive cells than did ventral prostate, and rat prolactin was more effective in demonstrating these binding sites than was ovine prolactin. Dorsal prostate epithelium was highly immunoreactive for binding of both ligands; however, there was considerably more staining in this lobe that remained after absorption of the antibody with prolactin. These data suggest that the inability to demonstrate prolactin binding sites in the lateral lobe using radioligand assay may have been due to the fewer numbers of binding sites that were diluted below the sensitivity of the assay when a tissue homogenate preparation was used. Noncompetitive binding in the dorsal lobe, as seen in the radioligand assay, coincided with immunocytochemical findings of relatively high nonabsorbable background staining.

Animals↗
PubMed1997

Effect of prolactin on the attractiveness of male odors to females in meadow voles: independent and additive effects with testosterone.

This study investigated the roles of testosterone and prolactin in seasonal changes in the attractiveness of odors of male meadow voles to long-photoperiod females. Prolactin was reduced in long-photoperiod males by treatment with bromocryptine (Experiment 1) and increased in short-photoperiod males by replacement with ovine prolactin (Experiment 2). Testosterone was manipulated by castration and testosterone replacement. During long photoperiods, the attractiveness of the odor produced by male meadow voles depends on the circulating titers of both prolactin and testosterone. Males with high titers of both hormones produced scents that were highly attractive to females; those with low titers of both hormones produced unattractive scents. When the concentration of one hormone was high and the other low, long-photoperiod males produced scents of intermediate attractiveness. During short photoperiods, the attractiveness of the male's scents depended strictly on his prolactin titers. Males with high prolactin titers produced attractive scents, and males with low prolactin titers produced unattractive scents, regardless of their prolactin concentrations. Thus, high titers of both testosterone and prolactin are needed to produce attractive scents in males exposed to long photoperiods, whereas high prolactin titers are sufficient in short-photoperiod males.

Animals↗
PubMed2000

The role of prolactin in the regulation of clutch size and onset of incubation behavior in the American kestrel.

In most bird species, the timing of incubation onset may influence the degree of hatching asynchrony, which, together with variation in clutch size, affects reproductive success. In some domesticated species that usually show no hatching asynchrony, plasma prolactin concentrations in females rise with the onset of incubation and the end of laying, and this rise enhances incubation behavior and may terminate laying. To investigate whether a rise in prolactin during laying is involved in the regulation of clutch size and incubation onset in a species with hatching asynchrony, we measured plasma concentrations of immunoreactive prolactin (ir-prolactin) in laying American kestrels, Falco sparverius, and quantified clutch size and incubation behavior. In a separate study, we administered one of three concentrations of ovine prolactin (o-prolactin) via osmotic pumps implanted in females when egg 2 of a clutch was laid. ir-Prolactin concentrations during laying were higher in small than in large clutches and increased in parallel with the development of incubation behavior. o-Prolactin treatment enhanced incubation behavior, but did not affect clutch size, possibly because the manipulation was performed after clutch size had already been determined. Consistent with studies on domesticated species that show synchronous hatching, our results indicate that rising prolactin during laying enhances the expression of incubation behavior in a species that shows hatching asynchrony. Further studies are necessary to determine whether the relationship between prolactin and clutch size in the American kestrel is one of causation or of mere association.

Animals↗
PubMed2000

High-level expression of biologically active human prolactin from recombinant baculovirus in insect cells.

We examined the feasibility of high-level production of recombinant human prolactin, a multifunctional protein hormone, in insect cells using a baculovirus expression system. The human prolactin cDNA with and without the secretory signal sequence was cloned into pFastBac1 baculovirus vector under the control of polyhedrin promoter. Prolactin was produced upon infection of either Sf9 or High-Five cells with the recombinant baculovirus containing the human prolactin cDNA. The production of recombinant prolactin varied from 20 to 40 mg/L of monolayer culture, depending on the cell types. The prolactin polypeptide with its own secretory signal was secreted into the medium. N-terminal amino acid sequence analysis of the recombinant polypeptide purified from the culture medium indicated that the protein was processed similar to human pituitary prolactin. Carbohydrate analysis of the purified protein indicated that a fraction of the recombinant prolactin made in insect cells appeared to be glycosylated. Also, both secreted and nonsecreted forms of the recombinant prolactin in insect cells were biologically equivalent to the native human prolactin (pituitary derived) in the Nb2 lymphoma cell proliferation assay.

Animals↗