Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, we demonstrated that repeated treatment with recombinant human prolactin (rhPRL) protected mice against Salmonella typhimurium infection. The protective activity was statistically significant, dose-dependent and present only when rhPRL treatments were performed before the infection. This activity was probably related to the observed increases in phagocytosis and intracellular killing of peritoneal macrophages induced by the hormonal treatment. The number of peripheral leukocytes was not modified, excluding a mobilization of cells from other compartments. A decrease in the mortality rate after challenge was also observed in mice treated with the monoclonal antibody anti-PRL receptor U5, confirming that the protective activity was associated with receptor activation. Our studies also suggest that nitric oxide (NO) production was involved in the protective effect of rhPRL since pre-treatment of the animals with L-NAME, an inhibitor of NO-synthase, was able to completely revert the protective activity, whereas D-NAME, the inactive D-isomer, was without effect.
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PMID:Recombinant human prolactin induces protection against Salmonella typhimurium infection in the mouse: role of nitric oxide. 888 Feb 20

In order to establish whether nitric oxide (NO) is involved in the regulation of basal and/or TRH- or metoclopramide (MCP)-stimulated PRL secretion, normal male subjects were treated i.v. with the NO-synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) (40 mg/kg injected plus 50 mg/kg infused over 60 min) in basal conditions (N.7 subjects) or just before the PRL releasing hormone TRH (20 or 200 microg iv) (N.7 subjects) or the antidopaminergic agent MCP (1 or 10 mg iv) (N.7 subjects). In control experiments, subjects received normal saline instead of L-NAME. The administration of L-NAME modified neither the basal secretion of PRL, nor the PRL release induced by TRH (20 or 200 microg) or MCP (1 or 10 mg). These data suggest that in humans, NO is not involved in the control of PRL release at the anterior pituitary level.
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PMID:Effect of nitric oxide on basal and TRH-or metoclopramide-stimulated prolactin release in normal men. volpi@ipruniv.cce.unipr.it. 992 Apr 55

Pituitary adenomas are common benign neoplasms, accounting for approximately 15% of intracranial tumors. In systematic autopsy, pituitary tumors are found in 25%, of the population, but only one-third of these tumors give rise to clinical manifestations. Why most of these neoplasms remain undiagnosed and pituitary carcinomas are extremely rare? The progress in the studies concerning pituitary tumorigenesis is rather slow and, due to several limitations, including the anatomic inaccessibility of human pituitary gland, the lack of functional human cell lines in culture and the discrepancies between human and animal pituitary oncogenesis (in rodents pituitary hyperplasia is a prerequisite for adenoma development). In humans, the majority of pituitary tumors are monoclonal in origin and derived from single mutated pituicyte, rarely hyperplasia is a prerequisite for adenoma formation. As in the case of other tumors, activating mutations in oncogenes (GNAS1, PTTG) and inactivating mutations in tumor suppressor genes (MEN1, CNC1) lead to pituitary tumors development. However, mutations in classic oncogenes are very rarely associated with these tumors. Moreover, the important role of some hypothalamic hormones, peripheral hormones and their receptors (e.g. GHRH, dopamine D2 receptor, PRL receptor, estrogens, thyroid hormone receptor) and growth factors (e.g. FGF, EGF, TGF) is postulated and partially proved in promotion of pituitary tumorigenesis. Further studies are required to determine which of these events are truly primary changes in pituitary tumorigenesis, what may allow development of gene therapy.
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PMID:[Molecular aspects of pituitary tumors]. 1635 Jul 28

The available evidence points to participation of PRL in regulation of mammalian oocyte maturation. The aim of the present study was to characterize pathways of PRL action on bovine oocytes. We analyzed (1) the presence of the PRL receptor and its mRNA isoforms in oocytes and cumulus cells; (2) the effect of PRL on meiosis resumption and the role of cumulus cells, the NO/NO synthase system, protein kinase C, and tyrosine kinases in this effect; and (3) PRL effects in the presence of gonadotropins on the developmental capacity of cumulus-free and cumulus-enclosed oocytes. The transcript and protein expression of the PRL receptor in the cells were detected by reverse transcription polymerase chain reaction and immunocytochemistry, respectively. The nuclear status of oocytes was assessed after culture of cumulus-oocyte complexes (COCs) and denuded oocytes (DOs) with or without PRL (5-500 ng/mL) for 7, 14, or 24 hours. Besides, DOs were incubated for 7 hours in the absence or the presence of PRL (50 ng/mL) and/or L-NAME (an inhibitor of NO synthase), genistein (an inhibitor of tyrosine kinases), or calpostin C (a protein kinase C inhibitor). After IVM in 2 different systems containing PRL (50 ng/mL) and/or gonadotropic hormones, a part of oocytes underwent IVF and IVC and the embryo development was tracked until the blastocyst stage. Messenger RNA of long and short isoforms of the PRL receptor was revealed in both oocytes and cumulus cells. Immunocytochemistry confirmed the presence of the PRL receptor in oocytes and the cumulus investment. In the absence of gonadotropins (system 1), PRL retarded meiosis resumption in DOs but not in cumulus-enclosed oocytes, with this effect being short term, dose dependent, suppressed by L-NAME and genistein, and unaffected by calpostin. In systems containing gonadotropins, PRL did not affect nuclear maturation and the cleavage rate of cumulus-free and cumulus-enclosed oocytes. However, in the case of COCs, it raised the blastocyst yield both in system 2 (from 20.5%-40.9%, P < 0.01) and in system 3 (from 21.7%-33.9%, P < 0.05). The findings show for the first time the functioning of the direct pathway of PRL signaling into bovine oocytes, as confirmed by the expression of receptors of PRL and its direct meiosis-retarding effect involving activation of tyrosine kinases and NO synthase. Furthermore, this is the first demonstration that the beneficial effect of PRL on the oocyte developmental capacity is achieved via cumulus cells containing PRL receptors.
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PMID:Prolactin affects bovine oocytes through direct and cumulus-mediated pathways. 2521 95