Relevant bibliographies by topics / Prolactin

Academic literature on the topic 'Prolactin'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Prolactin"

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Chastel, Olivier, and Hervé Lormée. "Patterns of Prolactin Secretion in Relation to Incubation Failure in a Tropical Seabird, the Red-Footed Booby." Condor 104, no. 4 (November 1, 2002): 873–76. http://dx.doi.org/10.1093/condor/104.4.873.

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Abstract Prolactin levels rapidly drop after breeding failure in several terrestrial bird species, but in penguins prolactin secretion can be maintained well after failure. We measured prolactin secretion in relation to reproductive failure in a tropical seabird, the Red-footed Booby (Sula sula). Incubation failure was recorded in 7 nests (2 accidental losses, 5 desertions). Prolactin titers significantly decreased after incubation failure. In birds that accidentally lost their egg, prolactin titers declined but measurements 12 to 24 hr after failure were still above basal levels. Birds naturally deserting their egg exhibited prolactin titers typical of basal levels 6–24 hr after abandonment. Two birds showed lower prolactin concentration as early as 4–8 days before nest desertion, suggesting that a decline in prolactin levels may precede egg desertion. This study shows that in this tropical seabird, incubation failure results in a rapid cessation of prolactin secretion, as it does for terrestrial birds. Relación entre los Niveles de Prolactina y el Fracaso Reproductivo en un Ave Marina Tropical, Sula sula Resumen. Los niveles de prolactina de varias especies de aves terrestres disminuyen rápidamente después del fracaso reproductivo. Sin embargo, en los pingüinos la secreción de prolactina tiende a mantenerse inalterada después del fracaso reproductivo. Medimos los niveles de prolactina en relación al fracaso reproductivo en un ave marina tropical, Sula sula. Se observaron 7 eventos de fracaso reproductivo (2 pérdidas accidentales de huevos y 5 deserciones de nidos). En general, los niveles de prolactina disminuyeron significativamente después del fracaso reproductivo. En las aves que perdieron accidentalmente sus huevos, los niveles de prolactina disminuyeron, pero las medidas registradas 12 a 24 horas después del fracaso fueron superiores a los niveles basales. Los niveles de prolactina de individuos que espontáneamente abandonaron sus nidos, medidos 6 a 24 horas después del abandono, fueron similares a los niveles basales. Dos individuos presentaron concentraciones de prolactina bajas 4 a 8 días antes del abandono de sus nidos, sugiriendo que una disminución del nivel de prolactina podría preceder el abandono de los nidos. Este estudio demuestra que el fracaso de incubación de esta especie de ave marina tropical conlleva a una rápida cesación de la secreción de prolactina, tal como ha sido observado en las aves terrestres.
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Jerry, D. J., L. C. Griel, J. F. Kavanaugh, and R. S. Kensinger. "Binding and bioactivity of ovine and porcine prolactins in porcine mammary tissue." Journal of Endocrinology 130, no. 1 (July 1991): 43–51. http://dx.doi.org/10.1677/joe.0.1300043.

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ABSTRACT Differential binding of homologous and heterologous prolactin was investigated in porcine mammary tissue. Specific binding of ovine prolactin to porcine mammary membranes or tissue slices was significantly greater than specific binding of the homologous porcine prolactin. Ovine prolactin was also more potent than porcine prolactin in stimulating proliferation of Nb2 cells. In contrast, stimulation of glucose metabolism in porcine mammary explants by porcine prolactin was greater than that by ovine prolactin. Differences in specific binding were probably not due to damage during iodination, as low concentrations of iodinated prolactins were similar to unlabelled prolactins in their abilities to stimulate proliferation of Nb2 cells. Furthermore, electrophoretic analysis of medium from binding reactions suggested that differences in specific binding were not due to proteolytic cleavage of the homologous prolactin into large (> 10 kDa) fragments. These studies suggest that ovine prolactin either binds to sites in addition to the authentic lactogenic receptor in porcine mammary tissue or that a significantly higher affinity of ovine prolactin for the porcine lactogenic receptor has little effect on its biological activity. Journal of Endocrinology (1991) 130, 43–51
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3

Kim, B. G., and C. L. Brooks. "Isolation and characterization of phosphorylated bovine prolactin." Biochemical Journal 296, no. 1 (November 15, 1993): 41–47. http://dx.doi.org/10.1042/bj2960041.

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Quantitative isolation of bovine prolactin was accomplished by immunoaffinity chromatography using clonal antibody as the stationary ligand. The phosphorylated and non-phosphorylated (native) prolactins contained in the immunopurified preparations were separated by chromatofocusing. Isolates from individual pituitaries revealed that phosphorylated prolactin represented between 20 and 80% of the total prolactin. The stoichiometry of phosphate in phosphorylated prolactin was 1.4:1 when determined by amino acid analysis after preparation of the S-ethylcysteine derivative. One major phosphorylation site, serine-90, and two minor sites, serine-26 and -34, were determined by mapping and sequencing studies. Serine-90 was conserved in prolactins, growth hormones and placental lactogens. Serine-26 and -34 were conserved in prolactins, but were not found in growth hormones or placental lactogens. Absorption spectroscopy of the aromatic amino acid residues indicated that phosphorylation of prolactin was associated with a unique structural conformation.
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4

Kikuyama, S., T. Yazawa, S. Abe, K. Yamamoto, T. Iwata, K. Hoshi, I. Hasunuma, G. Mosconi, and A. M. Polzonetti-Magni. "Newt prolactin and its involvement in reproduction." Canadian Journal of Physiology and Pharmacology 78, no. 12 (December 1, 2000): 984–93. http://dx.doi.org/10.1139/y00-099.

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The amino acid sequence of newt (Cynops pyrrhogaster) prolactin deduced from the nucleotide sequence of its cDNA showed a relatively high homology with sequences of chicken and sea turtle prolactins as well as with those of anuran prolactins. Cynops prolactin receptor transcripts were detected in various tissues and organs, suggesting that prolactin plays multiple roles in urodeles. Urodele prolactin was purified from the pituitaries of C. pyrrhogaster. Antiserum against this prolactin was used for radioimmunoassay of plasma prolactin and immunoneutralization experiments. Endogenous prolactin was shown to induce migration to water, courtship behavior, and cessation of spermatocytogenesis in the Cynops newt. The hormone was found to be involved in the development of cloacal glands such as the lateral and abdominal glands, growth of the tail and Mauthner neurons, secretion of oviducal jelly, and enhanced synthesis of a female attracting pheromone (sodefrin), and responsiveness of the olfactory epithelium to sodefrin. In most of these cases, prolactin was found to act synergistically or antagonistically with sex steroids. We also discovered that hypersecretion of prolactin in the newts subjected to cold temperature was induced by hypothalamic stimulation rather than release from hypothalamic inhibition.Key words: prolactin, newts, reproduction.
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Sapin, R., E. Le Guyader, A. Agin, and F. Gasser. "Dosages de prolactine Elecsys® : transition Prolactin Prolactin II." Immuno-analyse & Biologie Spécialisée 23, no. 2 (April 2008): 103–8. http://dx.doi.org/10.1016/j.immbio.2007.12.003.

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Scammell, J. G., D. N. Luck, D. L. Valentine, and M. Smith. "Epitope mapping of monoclonal antibodies to bovine prolactin." American Journal of Physiology-Endocrinology and Metabolism 263, no. 3 (September 1, 1992): E520—E525. http://dx.doi.org/10.1152/ajpendo.1992.263.3.e520.

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The epitopes recognized by three monoclonal antibodies generated to sheep prolactin were determined by evaluating their cross-reactivities by immunodot analysis with 14 mutants of bovine prolactin, in which individual amino acids had been deleted or substituted. Mutations were made throughout the molecule and included disruption of the amino-terminal, carboxyl-terminal, and central disulfide loops. Lack of immunoreactivity was taken as an indication that the site of mutation was part of the epitope. Antibody 6F11 reacted with all bovine prolactin mutants tested, except those in which the carboxyl-terminal cysteine (position 199) was substituted by a serine. Antibodies 5G2 and 4C10 reacted with all of the bovine prolactin mutants, except those in which the amino-terminal cysteine (position 4) was substituted by a serine. Western blot analysis of sheep, squirrel monkey, and rat prolactins with the monoclonal antibodies revealed that 5G2 and 4C10 were specific for sheep prolactin, whereas antibody 6F11 cross-reacted with prolactins from all three species. The mitogenic activity of sheep or rat prolactin in the Nb2 bioassay was determined in the presence of the antibodies to determine whether the epitopes were part of the functional domains of these prolactins. The bioactivity of sheep prolactin (0.4 ng/ml) was unaffected by the monoclonal antibodies [0.01-1 microgram immunoglobulin G (IgG)/ml], whereas the bioactivity of rat prolactin (1.25 ng/ml) was inhibited by 6F11 with an apparent 50% inhibitory concentration of 0.25 microgram IgG/ml. These results indicate that monoclonal antibodies 5G2 and 4C10 cross-react with a species-specific region of the amino-terminal disulfide loop of bovine prolactin.(ABSTRACT TRUNCATED AT 250 WORDS)
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Arámburo, C., J. L. Montiel, J. A. Proudman, L. R. Berghman, and C. G. Scanes. "Phosphorylation of prolactin and growth hormone." Journal of Molecular Endocrinology 8, no. 3 (June 1992): 183–91. http://dx.doi.org/10.1677/jme.0.0080183.

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ABSTRACT To determine whether GH and prolactin could be phosphorylated, turkey GH, chicken GH, chicken prolactin and turkey prolactin were incubated in vitro with the catalytic subunit of protein kinase A and [γ-32P]ATP. Phosphorylation was assessed after sodium dodecyl sulphate-polyacrylamide gel electrophoresis, Western blotting and autoradiography. Polyacrylamide electrophoresis showed that both purified native chicken GH and turkey GH were phosphorylated under the conditions employed. However, the glycosylated variant of chicken GH did not appear to be labelled. Chicken prolactin, turkey prolactin and the glycosylated variant of turkey prolactin were all intensely phosphorylated by protein kinase A. Ovine and rat prolactins could also be phosphorylated by protein kinase A. The phosphate content of different native prolactin (turkey, ovine and rat) and GH (ovine and chicken) preparations was also determined and found to be significant. Chicken pituitary cells in primary culture incorporated P in GH- and prolactin-like bands isolated by non-denaturing polyacrylamide gel electrophoresis, and this was stimulated by phorbol myristate acetate. Phosphorylation of GH and prolactin may thus explain some of the charge heterogeneity of these hormones.
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Takahashi, N., K. Yamamoto, and S. Kikuyama. "Cloning of a toad prolactin cDNA: expression of prolactin mRNA in larval and adult pituitaries." Journal of Molecular Endocrinology 11, no. 3 (December 1993): 343–49. http://dx.doi.org/10.1677/jme.0.0110343.

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ABSTRACT A toad (Bufo japonicus) prolactin cDNA was specifically amplified from cDNAs constructed from the total RNA of adenohypophyses, employing the DNA polymerase chain reaction. Sequencing analysis revealed that the cDNA clone thus obtained was 602 bp in length, and encoded the C-terminal 134 amino acid residues of the toad prolactin molecule. The length of the toad prolactin mRNA was estimated to be about 1·0 kb by Northern blot analysis. The partial amino acid sequence deduced from the nucleotide sequence showed the following homologies between toad prolactin and the prolactins of other vertebrates: 69% with man, 80% with chicken, 81% with sea turtle, 91% with bullfrog and 38% with salmon. Using the cDNA as a probe, developmental and seasonal changes in prolactin mRNA levels in the pituitaries of toads were studied. Prolactin mRNA in the pituitary rose as metamorphosis progressed and declined at the end of metamorphosis. During the breeding season the pituitary content of prolactin mRNA was relatively high. This finding suggests that the increases in plasma and pituitary prolactin levels in larvae at metamorphic climax and in adults that remain in or migrate into water, as reported previously, accompany the increase in prolactin synthesis.
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Gabou, L., M. Boisnard, I. Gourdou, H. Jammes, J.-P. Dulor, and J. Djiane. "Cloning of rabbit prolactin cDNA and prolactin gene expression in the rabbit mammary gland." Journal of Molecular Endocrinology 16, no. 1 (February 1996): 27–37. http://dx.doi.org/10.1677/jme.0.0160027.

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ABSTRACT cDNA clones coding for rabbit prolactin were isolated from a pituitary library using a rat prolactin RNA probe. One cDNA contained 873 bases including the entire coding sequence of rabbit prolactin, its signal peptide and the 5′ and 3′ untranslated regions of 44 and 145 nucleotides respectively. The deduced amino acid sequence of the cloned prolactin cDNA presented a 93–78% identity with mink, porcine and human prolactins. The prolactin gene transcription was investigated by RT-PCR analysis in several organs of midlactating New Zealand White rabbits. The ectopic transcription of the prolactin gene was examined in more detail in the mammary gland. A strong PCR signal was detected in the mammary gland of virgin does and was also observed during pregnancy and at the beginning of lactation. This PCR signal was very weak in mid-lactating and absent in post-weaning mammary gland.
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Carnevali, O., G. Mosconi, K. Yamamoto, T. Kobayashi, S. Kikuyama, and A. M. Polzonetti-Magni. "In-vitro effects of mammalian and amphibian prolactins on hepatic vitellogenin synthesis in Rana esculenta." Journal of Endocrinology 137, no. 3 (June 1993): 383–89. http://dx.doi.org/10.1677/joe.0.1370383.

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ABSTRACT Male and female Rana esculenta liver was induced in an in-vitro system by homologous and Rana catesbeiana pituitary to synthesize and release vitellogenin, a lipoglycophosphoprotein precursor of yolk proteins, lipovitellins and phosvitins, in oviparous vertebrates. In the present experiments, the action of prolactin on hepatic vitellogenin synthesis and release was investigated, using ovine prolactin and Rana catesbeiana prolactin. The effects of prolactin on hepatic vitellogenin synthesis displayed different trends related to sex; male liver was found to be more responsive than female liver to both ovine and frog prolactin; moreover, the response to prolactin was dose-related (r = 0·998; P <0·05) in male but not in female liver. In both sexes, a high degree of seasonality in the responsiveness of the liver was found, since the vitellogenin levels induced by prolactin during the winter phase were significantly (P < 0·001) higher than those produced during the summer phase. Thus, there was no significant difference between the action of ovine and frog prolactin on vitellogenin synthesis; in fact, mammalian prolactins are structurally similar with regard to nucleotide and amino acid sequences. The direct action of prolactin on hepatic vitellogenin synthesis in the frog Rana esculenta is discussed, on the basis of the role played by prolactin as an important growth modulatory hormone in fetal and adult tissues. Journal of Endocrinology (1993) 137, 383–389
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Dissertations / Theses on the topic "Prolactin"

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Bernard, Valérie. "Rôle de la prolactine dans la tumorigenèse du prolactinome." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS280.

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Nous avons souhaité, dans ce travail de Thèse, préciser le rôle de l’hormone prolactine (PRL) dans la tumorigenèse des prolactinomes. Nous avons tout d’abord décrit l’histoire naturelle et moléculaire des tumeurs lactotropes développées par le modèle de souris Prlr-/-, invalidé de façon globale pour le récepteur de la PRL (PRLR). Les femelles Prlr-/- développent des prolactinomes avec 100% de pénétrance à 12 mois. Ces tumeurs sont très sécrétantes, invasives et prolifératives. L’analyse transcriptomique comparative des hypophyses de souris Prlr+/+ et Prlr-/- nous a permis de mettre en évidence de nouvelles voies de signalisation impliquées dans la survenue de ces tumeurs. Ces nouveaux gènes candidats seront à rechercher chez l’Homme. Par ailleurs, l’étude d’un autre modèle murin développé dans le cadre de ce travail, invalidé de façon spécifique dans la cellule lactotrope, a permis de démontrer pour la première fois in vivo que la PRL exerçait un rétrocontrôle autocrine sur la sécrétion et la prolifération des cellules lactotropes. Bien que nous n’ayons pas retrouvé de mutation germinale du PRLR dans une large cohorte de patients atteints de prolactinome sporadique, nos résultats suggèrent que des mutations somatiques de ce gène ne sont pas à exclure et pourraient contribuer à la survenue de la pathologie humaine
In this work, we investigated the role of prolactin (PRL) in prolactinoma tumorigenesis. We first described the natural and molecular history of lactotroph cell tumors developed by the Prlr-/- mouse model, globally invalidated for the PRL receptor (PRLR). The Prlr-/- females develop prolactinomas with 100% penetrance at 12 months of age. These tumors are highly secreting, invasive and proliferative. The comparative transcriptomic analysis of pituitaries from Prlr+/+ and Prlr-/- mice suggested new signaling pathways involved in lactotroph adenoma developement in this mouse model. The role of these novel candidate genes remains to be demonstated in Humans. Furthermore, by studying another mouse model developed during this work, deleted for Prlr only in lactotroph cells, we demonstrated for the first time that PRL exerts an autocrine feedback on lactotroph cell secretion and proliferation in vivo. Although we did not find any germline mutation of PRLR in a large cohort of patients with sporadic prolactinoma, our results suggest that somatic mutations of this gene cannot be excluded and may contribute to the onset of the human pathology
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Gordon, Timothy Jason. "THE BIOLOGICAL, STRUCTURAL AND KINETIC PROPERTIES OF PROLACTIN, PROLACTIN RECEPTOR ANTAGONISTS, GROWTH HORMONE AND THE PROLACTIN RECEPTOR." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1366356833.

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Ueda, Eric Kinnosuke Martins. ""Prolactina humana pseudofosforilada (S179D-hPRL) é um potente fator anti-angiogênico in vitro e in vivo"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/85/85131/tde-28052007-162443/.

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S179D prolactina (hPRL) é uma mímica molecular da prolactina humana fosforilada. Demonstrou-se que a S179D-hPRL era anti angiogênica nos ensaios de angiogênese baseados na membrana corialantóica de galinha e na córnea de camundongos. Investigações posteriores realizadas empregando modelos in vitro demonstraram que o tratamento com S179D-hPRL diminuiu o número de células viáveis, reduziu a formação de túbulos em Matrigel e interferiu com a migração e invasão da matriz extracelular. A análise dos fatores de crescimento de células endoteliais humanas tratadas com S179D-hPRL revelou: uma diminuição na expressão ou liberação da PRL endógena, da heme-oxigenase-1, do fator de crescimento de fibroblasto básico (bFGF) e um aumento na expressão de dois inibidores teciduais de metaloproteases. A S179D-hPRL também bloqueou a sinalização provocada por bFGF nessas células. Nós concluímos que essa mímica molecular do hormônio pituitário fosforilado é uma potente proteína anti-angiogênica, em parte devido á sua habilidade de reduzir o estímulo autócrino de fatores de crescimento de células endoteliais de cordão umbilical humano (HUVEC), por sua capacidade de bloquear a sinalização promovida pelo bFGF e por sua habilidade de interferir na migração endotelial. Também foi estudada a influência da S179D-hPRL na apoptose em células endoteliais humanas, empregando caspase-8 como um marcador da via extrínseca, e a liberação de citocromo C como um marcador da via intrínseca. As duas cascatas convergem na ativação da caspase-3, que cliva a fator de fragmentação de DNA (DFF45). Uma incubação de três dias com 50 ng/mL de S179D-hPRL quadruplicou o número de células apoptóticas; esse efeito duplicou-se com uma concentração de 100 ng/mL e atingiu um ápice com 500 ng/mL. A clivagem de DFF45 e da pro-caspase-8 foi detectado com 100 ng/mL. Citocromo C, porém, só foi observado com concentrações de 500 ng/mL. O regulador de ciclo celular p21 (um marcador pró-apoptótico) elevou-se com 100 ng/mL, enquanto que um incremento do supressor tumoral p53 necessitou três vezes o tempo de incubação e 500 ng/mL. A atividade do promotor de p21 foi máxima com 50 ng/mL do análogo de hPRL, enquanto que 500 ng/mL foram necessários para se visualizar uma alteração significativa na atividade do promotor de Bax (um indicador da atividade de p53). Como previamente demonstrado na literatura, S179D-hPRL bloqueou a fosforilação da quinase regulada extracelularmente (ERK) em resposta ao bFGF, mas também causou uma ativação tardia e prolongada da ERK. PD 98059 [inibidor específico da proteína quinase ativada por mitógeno (MAPkinase)] inibiu essa ativação tardia e sustentada assim como outros efeitos da S179D-hPRL, exceto aquele sobre a indução de p53 e ativação do promotor de Bax. Podemos concluir que baixas doses de S179D-hPRL bloqueiam a sinalização de ERK induzida por bFGF e concomitantemente ativam a ERK em um tempo diferente, resultando na elevação de p21 e ativando a via extrínseca de apoptose. Maiores tempos de incubação e concentração, entretanto, ativam a via intrínseca empregando uma cascata intracelular diferente. Esses achados sugerem que níveis circulantes de PRL fosforilada podem inibir a progressão do câncer e, portanto, S179D-hPRL poderia ser um agente anti-angiogênico útil na terapêutica.
S179D-prolactin (hPRL) is an experimentally useful mimic of naturally phosphorylated human prolactin. S179D-hPRL, but not unmodified PRL, was found to be anti-angiogenic in both the chorioallantoic membrane and corneal assays. Further investigation using human endothelial in vitro models showed reduced cell number, reduced tubule formation in Matrigel, and reduced migration and invasion, as a function of treatment with S179D-hPRL. Analysis of growth factors in human endothelial cells in response to S179D-hPRL showed a decreased expression or release of endogenous PRL, heme-oxygenase-1, basic fibroblast growth factor (bFGF), angiogenin, epidermal growth factor and vascular endothelial growth factor and an increased expression of inhibitors of matrix metalloproteases. S179D-hPRL also blocked signaling from bFGF in these cells. We conclude that this molecular mimic of a pituitary hormone is a potent anti-angiogenic protein, partly as a result of its ability to reduce utilization of several well-established endothelial autocrine growth loops, partly by its ability to block signaling from bFGF and partly because of its ability to decrease endothelial migration. We also examined the influence of S179D-hPRL on apoptosis in human endothelial cells, using procaspase-8 as a marker of the extrinsic pathway, and cytochrome C release as a marker of the intrinsic pathway. Both pathways converge at caspase-3, which cleaves DNA fragmentation factor (DFF45). A 3-day incubation with 50 ng/ml S179D-hPRL quadrupled the early apoptotic cells; this effect was doubled at 100 ng/ml and maximal at 500 ng/ml. DFF45 and pro-caspase 8 cleavage were detectable at 100 ng/ml. Cytochrome C, however, was unaffected until 500 ng/ml. p21 increased at 100 ng/ml, whereas a change in p53 activity required both triple the time and 500 ng/ml. p21 promoter activity was maximal at 50 ng/ml, whereas 500 ng/ml were required to see a significant change in the Bax promoter (a measure of p53 activity). As previously shown, S179D-hPRL blocked extracelular regulated kinase (ERK) phosphorylation in response to bFGF, but, in addition, continued co-incubation showed a delayed and prolonged activation of ERK. PD98059 [a specific mitogen-activated protein kinase (MAPkinase) inhibitor] inhibited this delayed activation of ERK and the effects of S179D-hPRL on all parameters except p53, or activity of the Bax promoter. We conclude that low doses of S179D-hPRL block bFGF-induced ERK signaling and yet activates ERK in a different time frame to elevate p21, and activate the extrinsic pathway. Longer incubations and higher concentrations, however, additionally activate the intrinsic pathway using an alternate intracellular signal. These findings suggest that circulating levels of phosphorylated hPRL may reduce the progression of cancer and, furthermore, that S179D-hPRL may be a useful anti-angiogenic therapeutic.
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4

Furigo, Isadora Clivatti. "Estudo do mecanismo de ação da bromocriptina e de antagonistas de prolactina no tratamento do Diabetes Mellitus tipo 2 e da obesidade." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-16052017-145647/.

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Atualmente, é crescente o interesse em estudar o potencial do Sistema Nervoso Central (SNC) como alvo de medicamentos antidiabéticos, uma vez que ele possui receptores de insulina e desempenha papel crítico na regulação da homeostase glicêmica. Nesse sentido, o Cycloset® (mesilato de bromocriptina de liberação rápida), um medicamento de ação central aprovado nos Estados Unidos para o tratamento do DMT2, atende a essa tendência atual. Trabalhos prévios mostram efeitos benéficos da bromocriptina (Bromo) sobre a hiperglicemia e hiperlipidemia em modelos de animais obesos tratados com essa droga. Por ser um agonista dopaminérgico, um dos possíveis mecanismos de ação dessa droga pode ser bloqueando a liberação e produção de prolactina (Prl). Níveis elevados de prolactina na circulação sanguínea, observados tanto em indivíduos com prolactinomas como em pessoas tratadas com medicamentos que causam hiperprolactinemia, geram anormalidades no metabolismo de carboidratos e lipídeos, o que pode levar a um quadro de síndrome metabólica. Na presente tese, testamos a hipótese de que ao menos parte dos efeitos antidiabéticos da Bromo seja mediada pela inibição da secreção de prolactina. Avaliamos os efeitos do tratamento com Bromo em camundongos machos e fêmeas geneticamente obesos e resistentes à insulina (ob/ob), bem como testamos se os efeitos benéficos do medicamento seriam revertidos com a reposição de Prl. Machos tratados com Bromo apresentaram maior sensibilidade à insulina, enquanto que a reposição de Prl manteve os animais menos sensíveis, tais como os animais do grupo controle. As fêmeas tratadas com Bromo apresentaram tendência à melhora de sensibilidade à insulina, bem como foram mais tolerantes à glicose, sendo que a reposição de Prl em animais tratados com Bromo também reverteu o efeito benéfico do medicamento. Dessa forma, demonstramos que ao menos parte dos efeitos antidiabéticos da Bromo é mediada pela inibição da secreção basal de Prl. Em um segundo conjunto de experimentos, testamos se a administração de antagonistas de prolactina (G129R-hPrlR) em machos ob/ob, por vias centrais ou periféricas, produziria efeito antidiabético. Observamos que tanto o tratamento periférico como o central diminui a curva glicêmica dos animais em testes de tolerância à glicose e melhoram a sensibilidade à insulina, embora ainda não tenhamos obtido valores significativos devido a nossa amostragem. Por fim, investigamos se a ação da Prl sobre o metabolismo ocorre por meio da interação com o receptor de estrógeno alfa (ERα). Verificamos que receptores de prolactina e de ERα são expressos em áreas comuns no SNC e que variações nos níveis circulantes de estrógeno causam mudanças na sensibilidade à prolactina. Portanto, no presente trabalho, identificamos o possível mecanismo pelo qual a Bromocriptina promove melhorias no controle glicêmico e, de forma inédita, produzimos evidências que o uso de antagonistas de prolactina pode ter potencial no tratamento do DMT2.
Type 2 Diabetes mellitus (T2DM) is a syndrome characterized by dysfunctions in the metabolism of glucose, amino acids and free fat acids. Although most of the drugs currently used to treat T2DM targets peripheral organs, a growing interest in studying the Central Nervous System (CNS) as a potential target of antidiabetic drugs is appearing. The CNS possesses insulin receptors and plays a critical role in regulating glucose homeostasis. In this sense, Cycloset® (quick release bromocriptine mesylate) a drug that acts on CNS, was recently approved in United States to treat T2DM. Previous studies have shown beneficial effects of bromocriptine (Bromo) on hyperglycemia and hyperlipidemia in obese animal models. As a dopaminergic agonist, a possible mechanism of action of this drug could be caused by a decreased prolactin (Prl) production and release. High serum prolactin levels, as observed in patients bearing prolactinomas or individuals using drugs that induce hyperprolactinemia, generate abnormalities in carbohydrate and lipid metabolism, which can lead to metabolic syndrome. In the current thesis, we tested the hypothesis that part of bromocriptine antidiabetic effects is due to an inhibition of prolactin secretion. We evaluated Bromo effects in genetically obese and insulin resistant male and female mouse (ob/ob), as well as we tested whether replacing Prl could reverse the beneficial effects of Bromo. Males treated with Bromo showed lower insulin resistence, whereas Prl replacement decreased insulin sensitivity. Females treated with Bromo showed tendency towards an improvement in their insulin sensitivity and glucose tolerance. Prl replacement also reversed the beneficial effects of Bromo in this group. Thus, we demonstrated that at least part of the antidiabetic effects of Bromo is due to inhibition of Prl secretion. In another set of experiments, we tested whether central or peripheral treatment with prolactin antagonists (G129R-hPrlR) causes antidiabetic effects in ob/ob male mice. Both peripheral and central treatment decreased the glycemic curve during glucose and insulin tolerance tests, although we still did not obtain statistically significant values with our sample size. Lastly, we investigated whether metabolic Prl action occurs due to a putative interaction with estrogen receptor alpha (ERα). We found a wide co-expression between Prl receptor and ERα in the CNS. Additionally, changes in estrogen levels decrease prolactin sensitivity. Therefore, in the present study we identified the possible mechanism by which bromocriptine promotes improvements in glycemic control, and for the first time, we obtained evidence that the use of prolactin antagonists can have a potential effect in the treatment of T2DM.
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Amaral, Vinícius Cestari do. "Expressão gênica da prolactina e seus receptores na hipófise e no útero de camundongo fêmea tratado com metoclopramida." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-18092012-114713/.

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INTRODUÇÃO: A prolactina é um hormônio polipeptídico, que possui reconhecida ação sistêmica, principalmente na fisiologia da reprodução, porém, seu desequilíbrio, em especial a hiperprolactinemia, é cada vez mais frequente na prática clínica. Apesar de ser um distúrbio relativamente comum, ainda existem dúvidas quanto aos efeitos moleculares da hiperprolactinemia no trato genital, particularmente no útero, e também na hipófise. O presente estudo teve por objetivo verificar os efeitos da hiperprolactinemia induzida pela metoclopramida na expressão gênica da prolactina e de seus receptores no útero e na hipófise de camundongo fêmea. MÉTODOS: Utilizaram-se 49 camundongos fêmeas (Wistar), randomicamente divididas em 7 grupos contendo 7 animais cada: 1) SS não ovariectomizadas que receberam solução salina (veículo); 2) M não ovariectomizadas tratadas com metoclopramida; 3) OSS ovariectomizadas tratadas com solução salina (veículo); 4) OM ovariectomizadas tratadas com metoclopramida; 5) OME ovariectomizadas tratadas com metoclopramida e 17-estradiol; 6) OMP ovariectomizadas tratadas com metoclopramida e progesterona micronizada; 7) OMEP ovariectomizadas tratadas com metoclopramida, 17-estradiol e progesterona micronizada. Após 50 dias os animais foram sacrificados sendo retirados o útero e a hipófise de cada animal para extração do ácido ribonucleico total, que foi utilizado para a síntese de ácido desoxirribonucleico complementar e avaliação da expressão gênica da prolactina e das diferentes isoformas de seus receptores, por reação em cadeia da polimerase em tempo real. RESULTADOS: Na hipófise, em animais não ovariectomizados, o tratamento com metoclopramida aumentou a expressão do gene que codifica a prolactina em relação ao tratamento apenas com o veículo. Nos animais castrados, a progesterona isoladamente ou associada ao estrogênio determinou o incremento do RNA mensageiro da prolactina em relação aos outros animais castrados que receberam outras combinações de tratamento. Este efeito foi semelhante ao da metoclopramida em animais com os ovários intactos. Em relação ao receptor de prolactina, o estrogênio e a progesterona, isoladamente, foram responsáveis pelo incremento da isoforma S2. No útero houve aumento na expressão de RNA mensageiro de prolactina após tratamento com metoclopramida ou com tratamento isolado ou combinado de estrogênio e progesterona. A ovariectomia determinou a redução da expressão das isoformas S1 e S2 do receptor de prolactina de todas as isoformas estudadas. Já o tratamento estroprogestativo determinou elevação da formas S3 e L do receptor, enquanto com a progesterona isoladamente causou apenas o incremento da forma L do receptor da prolactina no útero dos animais castrados. CONCLUSÕES: Nossos dados sugerem que o tratamento com metoclopramida altera de forma diferente a expressão de prolactina e de seus receptores quando se compara o resultado da hipófise em relação ao útero em camundongos fêmeas castrados e tratados com esteróides sexuais
INTRODUCTION: Prolactin is a polypeptide hormone with a recognized systemic action mainly on reproductive physiology. However, prolactin imbalance, particularly hyperprolactinemia, is increasingly more frequent in clinical practice. Although it is a comparatively common disorder, there are still doubts about the molecular effects of hyperprolactinemia on the genital tract especially in the uterus and the pituitary. The present study aimed at verifying the effects of metoclopramide-induced hyperprolactinemia on the gene expression of prolactin and its receptors in the uterus and pituitary of the female mouse. METHODS: Forty-nine female Wistar mice were randomized to 7 equal-sized groups as follows: 1) SS nonoophorectomized mice treated with saline solution (vehicle); 2) M nonoophorectomized mice treated with metoclopramide; 3) OSS oophorectomized mice treated with saline solution (vehicle); 4) OM oophorectomized mice treated with metoclopramide; 5) OME oophorectomized mice treated with metoclopramide and 17-estradiol; 6) OMP oophorectomized mice treated with metoclopramide and micronized progesterone; 7) OMEP oophorectomized mice treated with metoclopramide, 17-estradiol, and micronized progesterone. The animals were sacrificed 50 days after the end of the treatment, and the uterus and pituitary of each animal were removed for extraction of total ribonucleic acid, which was then used for synthesizing complementary deoxyribonucleic acid and for evaluating the gene expression of prolactin and the different isoforms of its receptors by the real-time polymerase chain reaction. RESULTS: In the pituitary of the nonoophorectomized mice, the treatment with metoclopramide against that with vehicle alone increased the expression of the prolactin-encoding gene. In the castrated animals, progesterone by itself or in conjunction with estrogen determined a raise in prolactin messenger RNA as opposed to the two other treatments with different combinations. This effect was similar to that produced by metoclopramide in animals with intact ovaries. Estrogen and progesterone, acting independently of each other, were responsible for the increase in the S2 isoform of the prolactin receptor. In the uterus, there was heightened expression of prolactin messenger RNA under the effect of the treatment with metoclopramide or with estrogen and/or progesterone. Oophorectomy caused a greater reduction in expression of the prolactin receptor S1 and S2 isoforms than in the other isoforms. However, the combined estrogen plus progesterone treatment led to an increase in the S3 and L forms of the receptor, while progesterone alone resulted solely in a higher expression of the L form of the prolactin receptor in the endometrium of the castrated mice. CONCLUSION: Our data suggest that metoclopramide treatment induces different changes in the expression of prolactin and its receptors according to whether the effect occurs in the pituitary or the uterus of castrated female mice treated with sex steroids
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Patmastan, Piyanuj. "Comparison of properties of wild-type human prolactin and a potent antagonist." Columbus, OH : Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1061248268.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xv, 163 p.: ill. (some col.). Includes abstract and vita. Advisor: Charles L. Brooks, Dept. of Veterinary Biosciences. Includes bibliographical references (p. 156-163).
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Gould, David R. (David Ross). "Prolactin in human breast cancer." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41006.

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The function of prolactin in human breast cancer was studied using four different approaches. First, purification and characterization of the prolactin receptor from breast cancer cells indicated that the receptor has a molecular mass of 88 000 Da, 67 000 Da being protein, and the other 21 000 Da presumably carbohydrate. Secondly, prolactin was tested for mitogenic activity in breast cancer in vitro. No consistent mitogenic response to prolactin could be demonstrated in these experiments. Thirdly studies upon the regulation of the prolactin receptor in breast cancer cells indicated that the prolactin receptor is stimulated by lactogen, estrogen and progesterone at the protein level. Estrogen, progesterone, thyroid hormone, and forskolin (but not lactogen) increase prolactin receptor steady state RNA levels, and the phorbol ester PMA and retinoic acid inhibited receptor RNA levels. However, effects at the RNA level were of a much lesser magnitude than effects at the protein level. Mechanisms other than transcriptional regulation alone are likely involved in prolactin receptor regulation. Fourthly, prolactin receptor and prolactin inducible protein/gross cystic disease fluid protein (PIP/GCDFP-15) RNA levels were examined in breast cancer tumors. Highly significant correlations were observed between the prolactin receptor and the progesterone receptor; the prolactin receptor and PIP/GCDFP-15; and PIP/GCDFP-15 and progesterone receptor.
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Amaya, Julieta Esperanza Ochoa. "Efeitos da hiperprolactinemia sobre a inflamação alérgica pulmonar em ratos Wistar." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-09052016-143242/.

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Objetivo: Foi investigada a hipótese da hiperprolactinemia modular a resposta inflamatória alérgica pulmonar em ratos machos e em fêmas lactantes sem tratamento de domperidona. Métodos: Em ratos machos, a hiperprolactinemia foi de curta duração (5 dias) induzida pela domperidona (5,1 mg.kg-1 por dia, i.p). A resposta alérgica foi gerada por sensibilização e desafios inalatórios com ovoalbumina. Foi feita contagem de leucócitos totais e diferenciados do lavado bronco alveolar (BAL), lavado medular femoral (BFL) e sangue; a percentagem de produção de muco e colageno no pulmão, níveis de corticosterona e prolactina e citocinas TNF-α, IL-4, IL-6, IL-10, em explantes de pulmão e IFNg no BAL, foram medidos. Pela citometria foram avaliadaos os receptores de prolactina; Resultados: Hiperprolactinemia de curta duração feita antes do desafio inalatório disminuiu a resposta alérgica pulmonar na contagem de leucócitos no lavado broncoalveolar. Esse tratamento reduziu a celularidade no BFL e a percentagem de muco e aumentou a expressão de citocinas IL-4, IL-6, IL-10, TNFα e da expressão do IFNg. Níveis altos de prolactina diminuiram o número de eosinófilos ao pulmão no BAL. Pela citometria revelou-se que além de ter menor número de granulócitos migrados ao pulmão, estes apresentaram maior expressão do número de receptores por granulócito para prolactina no grupo tratado com domperidona. Alterações similares foram reveladas em fêmeas lactantes como foi a diminuição nos leucócitos do BAL, e no número de células do BFL. O tratamento profilático diminuiu a resposta alérgica tanto no grupo hiperprolactinêmico como no grupo veículo. O tratamento feito após o desafio inalatório não evidenciou alterações relevantes nas variáveis medidas. Conclusões: A hiperprolactinemia de curta duração, feita após a sensibilização e antes da inalação diminui a resposta inflamatória no pulmão em ratos. Os resultados deste estudo demonstram que a hiperprolactinemia induzida antes do desafio antigênico diminue a inflamação alérgica pulmonar. Assim, é provável que a prolactina endógena tenha um papel relevante como um imunomodulador da asma. Este estudo aponta a possibilidade futura do uso da domperidona para pacientes asmáticos. Durante a primavera muitas espécies de mamíferos têm seus filhotes e ocorre abundância de fatores alergenos no ar. Logo, um fator endógeno que favoreça a proteção de fêmeas durante a lactação, tal como a hiperprolactinemia, tem elevado valor adaptativo
Objective: It was investigated if hyperprolactinemia has modulatory actions on lung allergic inflammatory response in male rats. Lactating female rats were tested for pulmonary allergy as well. Methods: In male rats, short-term (5 days) hyperprolactinemia was induced by domperidone (5.1 mg.kg-1 per day, ip). Allergic response was generated by sensitization and inhalation challenge with ovalbumin. Total and differential leukocytes bronchoalveolar lavage (BAL), femoral medullary lavage (BFL) and blood; the percentage of collagen and mucus production in the lungs, plasma levels of corticosterone and prolactin cytokines and TNF-α, IL-4, IL-6, IL-10, IFNg explants lung and BAL, were measured. Flow cytometry was used to evaluate prolactin receptor; Results: Short-term hyperprolactinemia made before the inhaled challenge reduced the pulmonary allergic response in white blood cell counts in BAL. This treatment reduced the cellularity in BFL and the percentage of mucus and increased expression of cytokines IL-4, IL-6, IL-10, TNFa and IFNg expression. High prolactin levels decreased the number of eosinophils to the lung in BAL. There were fewer granulocytes migrated to the lung. These granulocytes showed higher expression prolactin receptors in hyperprolactinemia animals. Similar changes were revealed in lactating females. In these animals, there was a reduction in BAL leukocyte, and the number of cells BFL. Prophylactic treatment decreased the allergic response in both hyperprolactinemic and vehicle groups. The treatment made after inhalational challenge did not induce significant changes in the variables measured in this study. Conclusions: Short-term hyperprolactinemia, made after sensitization and before inhalation, decreases the inflammatory response in the lung of rats. The results of this study demonstrate that hyperprolactinemia, induced before antigen challenge, decreases pulmonary allergic inflammation. Thus, it is probable that the endogenous prolactin has an important role as an immunomodulator of asthma. This study points out the prospect of a future use of domperidone for asthmatic patients. For various mammalian species, parturition occurs during springtime. Pollen in the air might be an abundant allergic factor during springtime. Thus, protecting lactating females against this type allergy might have high adaptive value
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Arthuso, Fernanda dos Santos. "Adaptação de células CHO secretoras de prolactina humana e seus antagonistas para o crescimento em suspensão." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/85/85131/tde-20062011-110202/.

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O Grupo de Hormônios do Centro de Biotecnologia do IPEN desenvolveu várias linhagens de células de ovário de hamster chinês (CHO) modificadas geneticamente e comprovadamente eficientes na expressão de proteínas heterólogas, dentre elas a prolactina humana (hPRL) e os análogos antagonistas de prolactina (S179D-hPRL e G129R-hPRL). No entanto, todas as linhagens para expressão são cultivadas em monocamadas e dependentes da presença de soro fetal bovino (SFB) no meio de cultivo para um crescimento eficiente. As células em suspensão apresentam um grande interesse industrial-farmacêutico, tanto pela facilidade de cultivo e ampliação de escala, como pela produtividade volumétrica. Desenvolvemos um protocolo para adaptação de células CHO para o crescimento em suspensão e também processos de produção em frascos spinners. Nesse trabalho foi realizada a adaptação das linhagens produtoras de hPRL; S179D-hPRL e G129R-hPRL para o crescimento em suspensão e em meio livre de SFB. Realizamos também a produção em escala laboratorial com as três linhagens adaptadas, assim como a correspondente purificação e caracterização de quatro proteínas heterólogas, incluindo a prolactina humana glicosilada (G-hPRL).
The Hormone Group of the Biotechnology Center of IPEN has developed different cells lines of genetically modified chinese hamster ovary cells (CHO) for the expression of heterologus protein like human prolactin (hPRL) and its analogs/antagonists (S179D-hPRL and G129R-hPRL). All cell lines for expression are however cultured in monolayer culture dish and depend on fetal bovine serum (FBS) in the medium for an efficient growth. Cells in suspension show a great industrial-pharmaceutical interest, especially for the cultivation facility and scale enlargement as well as for volumetric productivity. We developed a protocol for adapting CHO cells to suspension growth, in spinner flasks. The adaption of our cell lines producing hPRL; S179D-hPRL and G129R-hPRL to suspension growth and in serum-free medium was obtained. We also carried out laboratory scale production with the three suspension-adapted culture line cells and the corresponding purification and characterization of four heterologous proteins, including glycosylated human prolactin (G-hPRL).
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Constantino, Flávia Bessi. "Relativa influência da prolactina, sua inibição e combinação com testosterona sobre a próstata de ratos castrados comparação entre recrescimento glandular, diferenciação celular e atividade secretora /." Botucatu, 2017. http://hdl.handle.net/11449/148973.

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Orientador: Luis Antonio Justulin Junior
Resumo: A próstata é uma glândula do sistema genital masculino que possui grande importância na fertilidade. Estudos clássicos evidenciaram que para que se inicie o desenvolvimento prostático é necessário a presença de andrógeno produzido pelos testículos fetais. Porém, além da estimulação androgênica, estudos apontam para outros hormônios que também atuam na próstata como a Prolactina (PRL). PRL é um hormônio que é principalmente secretado por células lactotróficas da hipofise anterior e está envolvido em muitos processos biológicos, incluindo lactação e reprodução. Assim, investigamos se a modulação da sinalização PRL altera a morfofisiologia da próstata ventral (VP) em ratos castrados. Os ratos Sprague Dawley adultos (n = 6) foram castrados e após 21 dias divididos em 10 grupos experimentais: Castrado Controle (CC): animais castrados que não receberam tratamento; Castrado+testosterona (T): animais castrados que receberam T (4mg / kg); Castrado+PRL (PRL): animais castrados recebendo PRL (0,3 mg / kg); Castrado+T+PRL (TPRL): animais castrados que receberam associação de T e PRL; e Castrado+BR (BR): animais castrados que receberam Bromocriptina (BR) (0,4mg / kg). Grupo Controle: animais intactos (CTR). Os animais foram tratados durante 3 ou 10 dias consecutivos. Ao fim dos tratamentos, os animais foram anestesiados, eutanizados e a prostata ventral (VP) foi removida, pesada e processada para análise histológica e Western blot. O peso corporal não se alterou entre os grupos experiment... (Resumo completo, clicar acesso eletrônico abaixo)
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Books on the topic "Prolactin"

1

Horseman, Nelson D., ed. Prolactin. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5.

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D, Horseman Nelson, ed. Prolactin. Boston: Kluwer Academic Publishers, 2001.

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Tritos, Nicholas A., and Anne Klibanski, eds. Prolactin Disorders. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11836-5.

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Diakonova, PhD, Maria, ed. Recent Advances in Prolactin Research. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12114-7.

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Naliato, Erika C. O. Prolactinomas, prolactin, and weight gain. Hauppauge, N.Y: Nova Science Publishers, 2010.

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A, Rillema James, ed. Actions of prolactin on molecular processes. Boca Raton, Fla: CRC Press, 1987.

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1932-, Mizuno Masahiko, Mori H. 1941-, and Taketani Y. 1947-, eds. Role of prolactin in human reproduction. Basel: Karger, 1988.

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International, Congress on Prolactin (4th 1984 Charlottesville Va ). Prolactin: Basic and clinical correlates : proceedings of the IV International Congress on Prolactin under the patronage of the International Society of Neuroendocrinology in association with the International Society of Endocrinology, and held in Charlottesville, Virginia on June 27-29, 1984. Padova, Italy: Liviana Press, 1985.

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Turrone, Peter. Prolactin response with typical and "atypical" antipsychotics. Ottawa: National Library of Canada, 2000.

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E, Blackwell Richard, and Chang R. Jeffrey, eds. Prolactin-related disorders: Proceedings of a symposium. Florham Park, N.J: Macmillan Healthcare Information, 1987.

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Book chapters on the topic "Prolactin"

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Ben-Jonathan, Nira. "Hypothalamic Control of Prolactin Synthesis and Secretion." In Prolactin, 1–24. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_1.

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Lorenson, Mary Y., and Ameae M. Walker. "Structure-Function Relationships in Prolactin." In Prolactin, 189–217. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_10.

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Ormandy, Christopher J., Nelson D. Horseman, Matthew J. Naylor, Jessica Harris, Fiona Robertson, Nadine Binart, and Paul A. Kelly. "Mammary Gland Development." In Prolactin, 219–32. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_11.

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Kindblom, J., K. Dillner, J. Törnell, and H. Wennbo. "Actions of Prolactin in the Prostate Gland." In Prolactin, 233–45. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_12.

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Buckley, Arthur R. "Prolactin Regulation of Cell Proliferation and Apoptosis." In Prolactin, 247–64. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_13.

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Risk, Michael, and Geula Gibori. "Mechanisms of Luteal Cell Regulation by Prolactin." In Prolactin, 265–95. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_14.

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Sorenson, Robert L., and T. Clark Brelje. "Regulation of Pancreatic Islets by Prolactin, Growth Hormone and Placental Lactogen." In Prolactin, 297–316. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_15.

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Hooghe-Peters, Elizabeth L., Zeynep Dogusan, and Robert Hooghe. "In Vitro Effects of Prolactin on the Lympho-Hemopoietic System." In Prolactin, 317–39. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_16.

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Edery, Marc, Nadine Binart, Brigitte Bouchard, Vincent Goffin, and Paul A. Kelly. "Prolactin Receptors." In Prolactin, 341–53. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_17.

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Clevenger, Charles V., Michael A. Rycyzyn, Farhat Syed, and J. Bradford Kline. "Prolactin Receptor Signal Transduction." In Prolactin, 355–79. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1683-5_18.

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Conference papers on the topic "Prolactin"

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Nyante, SJ, JM Faupel-Badger, ME Sherman, MM Gaudet, RT Falk, AA Andaya, RM Pfeiffer, et al. "Abstract P3-12-05: Genetic Variation in Prolactin and Prolactin Receptor, and Relationships with Serum Prolactin Levels and Breast Cancer Risk." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p3-12-05.

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Hoenicke, U., S. Albrecht, G. Hoeffken, and M. Halank. "Prolactin and the 16-kDa N-Terminal Fragment of Prolactin in Patients with Pulmonary Hypertension." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4897.

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Moszkorzova, L., C. Dostal, J. Marek, Z. Lacinova, and L. Musilova. "FRI0137 Prolactin in systemic lupus erythematosus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.172.

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Bi, W. Linda, Sherry Iuliano, and Edward R. Laws. "Surgical Management of Prolactin Adenomas in Women." In Special Virtual Symposium of the North American Skull Base Society. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725361.

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AL-Azzawie, Adnan. "STUDY THE CORRELATION BETWEEN EXTRAPITUITARY PROLACTIN –1149 G/T PROMOTER POLYMORPHISM AND PROLACTIN LEVELS FOR SOME IRAQI INFERTILE WOMEN." In International Conference of Natural Science 2017. College of Basic Education, Charmo University, Chamchamal, Sulaimani/Iraq, 2018. http://dx.doi.org/10.31530/17007.

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dos Santos Dias, Wanderson, Gerson Perondi, Otávio Martins, Gabriel Greggianin, Luciano Basso, and Diego Zambonin. "TSH, prolactin and GH-secreting adenoma: case report." In XXXII Congresso Brasileiro de Neurocirurgia. Thieme Revinter Publicações Ltda, 2018. http://dx.doi.org/10.1055/s-0038-1672934.

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Prokopuk, A. I., K. V. Yurchankova, E. M. Shpadaruk, and R. M. Smolyakova. "ASSESSMENT OF HORMONAL STATUS WITH AN ESTABLISHED MOLECULAR-BIOLOGICAL PROFILE OF PATIENTS WITH BREAST CANCER OF DIFFERENT REPRODUCTIVE PERIOD." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-93-96.

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In the course of the study, it was found that the luminal A subtype in patients with breast cancer is associated in 100% of cases with increased blood levels of estradiol, progesterone, and prolactin. In the postmenopausal period, the luminal B (Her-2-positive) subtype is associated with a 100% increase in the concentration of the hormones estradiol and progesterone. In patients with preserved ovarian-menstrual function, luminal B (Her-2-positive) subtype in 37.5% of cases is associated with increased estradiol content. Luminal B (Her-2-negative) subtype is associated with increased blood levels of estradiol, progesterone, and prolactin in 100% of patients. The Her-2 / neu-positive subtype is associated with decreased serum estradiol levels in 33% of patients and decreased progesterone levels in 83% of patients. In patients with a triple-negative subtype, an increased content of estradiol and progesterone in the blood was diagnosed in 100% of patients.
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Maixnerová, Jana, Andrea Špolcová, Resha Matyšková, Miroslava Blechová, Iva Veselá, Blanka Železná, and Lenka Maletínská. "Specific binding of prolactin-releasing peptide analogues in pituitary cells." In XIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2009. http://dx.doi.org/10.1135/css200911069.

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Tran-Thanh, D., D. Tran-Thanh, N. Arneson, M. Pintilie, K. Warren, A. Bane, F. O'Malley, F. O'Malley, S. Done, and S. Done. "Amplification of the Prolactin Receptor Gene in Mammary Lobular Neoplasia." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4151.

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Boome, LC Te, PM Welsing, AA Eijsbouts, and FH Van den Hoogen. "AB0070 The effect of prolactin on disease activity in sle." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1224.

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Reports on the topic "Prolactin"

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Tan, Dunyong. Prolactin and Human Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada513058.

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Ben-Jonathan, Nira. Role of Mammary Prolactin in Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada301702.

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Bunnell, B. N., and W. B. Iturrian. Social Behavior, Prolactin and the Immune Response. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/ada224055.

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Dahl, Geoffrey E., Sameer Mabjeesh, Thomas B. McFadden, and Avi Shamay. Environmental manipulation during the dry period of ruminants: strategies to enhance subsequent lactation. United States Department of Agriculture, February 2006. http://dx.doi.org/10.32747/2006.7586544.bard.

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The project resulted from earlier observations that environmental factors, especially photoperiod and temperature, had profound effects on milk yield in dairy cattle during lactation. More recently we had determined that photoperiod manipulation during the dry period altered milk yield in the next lactation, and this was associated with shifts in circulating concentrations of prolactin; specifically exposure to short days during the dry period decreases prolactin but increases milk yield. Because prolactin is also affected by temperature, with heat stress causing an increase in prolactin similar to that of long day exposure, we focused our efforts on determining prolactin signaling provides a common pathway for generation of environmental effects on mammary growth, development and subsequent function during the dry period of dairy ruminants. Over the project period we made significant progress toward testing our hypotheses that (I): In cows, there is a discrete duration of time during the dry period in which exposure to short days will result in optimal enhancement of mammary development and milk yield in the following lactation, and that this effect is mediated through demonstrable changes in mammary gland development, prolactin signaling, and mammary gene expression; and (II): Modulation of photoperiod and temperature during the dry period will affect milk yield in goats in the subsequent lactation via shifts in nutrient and endocrine partitioning, and mammary gene expression, during the dry period and into lactation. Cows exposed to short days for only the final 21 days of the dry period did not produce more milk that those on long day or natural photoperiod when dry. However, cows on short days for the entire 60 days dry did produce more milk than the other 3 groups. This indicates that there is a duration effect of short day exposure on subsequent milk yield. Results of the second study in cows indicate that mammary growth increases differentially during the dry period under long vs. short days, and that short days drive more extensive growth which is associated with altered prolactin signaling via decreases in an suppressors of cytokine signaling that represent an inhibitory pathway to mammary growth. Evidence from the studies in Israel confirms that goats respond to short days during the dry period in a similar manner to cows. In addition, heat stress effects on during the dry period can be limited by exposure to short days. Here again, shifts in prolactin signaling, along with changes in IGF-I secretion, are associated with the observed changes in mammary function in goats. These results have a number of biological and practical implications. For dairy producers, it is clear that we can recommend that cows and goats should be on reduced light exposure during the dry period, and further, cows and goats should be cooled to avoid heat stress during that time. Environmental influences on mammary growth are apparent during the dry period, and those effects have persistent impact in the subsequent lactation. Prolactin signaling is a consistent mechanism whereby extended light exposure and heat stress may depress mammary growth and development during the dry period. Thus, the prolactin signaling system offers an opportunity for further manipulation to improve production efficiency in dairy ruminants.
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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada485255.

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Liby, Karen, and Nira Ben-Jonathan. 16 K Prolactin as an Angiogenic Inhibitor in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada391620.

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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada472476.

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Chen, Wen Y. Rational Design of Human Prolactin Receptor Antagonists for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada403330.

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Chen, Wen Y. Rational Design of Human Prolactin Receptor Antagonists for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada420951.

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Chen, Wen Y. Rational Design of Human Prolactin Receptor Antagonists for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada392598.

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