Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The secretion of many hormones, including oxytocin, vasopressin and growth hormone, is not constant but shows a day-night rhythm. The suprachiasmatic nucleus (SCN) is thought to generate most mammalian biological rhythms and previous studies have reported suprachiasmatic efferents to the paraventricular nucleus (PVN) and the supraoptic nucleus (SON). We used in vivo extracellular electrophysiological techniques to show that the SCN also sends direct and indirect neural projections to the arcuate nucleus (ARC). This projection consisted of both excitatory and inhibitory components and may contribute to the entrainment of the rhythm in growth hormone secretion to the day-night cycle. Some SCN neurones appear to project to both the SON and the ARC. The SCN in turn receives excitatory and inhibitory inputs from the ARC and the peri-nuclear zone of the SON (peri-SON), which may provide feedback information, as well as allowing nonphotic entrainment of the SCN, for example, in response to feeding. Our data thus suggest extensive two-way connections between the SCN and its target nuclei which may contribute to the generation of day-night neuroendocrine rhythms. They also suggest the existence of indirect retinal projections to the ARC and PVN. We further investigated the retinal projection to the SCN. We were unable to demonstrate a significant difference in retinal input to those suprachiasmatic cells which had efferent projections to particular hypothalamic targets (SON and/or ARC), and those which did not.
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PMID:Neural connections of hypothalamic neuroendocrine nuclei in the rat. 1084 8

The thyrnus provides an optimal cellular and humoral microenvironment for the development of immunocompetent T lymphocytes. Although yolk sac derived pre-T, committed hematopoietic stem cells enter the thymus using a homing receptor, the immigration process also requires secretion of a peptide, called thymotaxin by the cells of the reticulo-epithelial (RE) network of the thymic cellular microenvironment. The thymic RE cells are functionally specialized based on their location within the thymic microenvironment. Thus, although subcapsular, cortical, and medullary RE cells are derived from a common, endodermal in origin epithelial precursor cell, their unique location within the gland causes their specialization in terms of their immunophenotypical and in situ physiological properties. The subcapsular, endocrine, RE cell layer (giant or nurse cells) is comprised of cells filled with PAS positive granules, which also express A2B5/TE4 cell surface antigens and MHC Class I (HLA A, B, C) molecules. In contrast to the medullary RE cells, these subcapsular nurse cells also produce thymosins beta 3 and beta 4. The thymic nurse cells (TNCs) display a neuroendocrine cell specific immunophenotype (IP): Thy-1+, A2B5+, TT+, TE4+, UJ13/A+, UJ127.11+, UJ167.11+, UJ181.4+, and presence of common leukocyte antigen (CLA+). Medullar RE cells display MHC Class II (HLA-DP, HLA-DQ, HLA- DR) molecule restriction. These cells also contain transforming growth factor (TGF)-beta type II receptors and are involved in the positive selection of T cells. Transmission electronmicroscopic (TEM) observations have defined four, functional subtypes of medullary RE cells: undifferentiated squamous, villous and cystic. All subtypes were connected with desmosomes. The secreted thy nic hormones, thymulin, thymosin-alpha 1 and thymopoietin (its short form, thymopentin or TP5) were detected immunocytochemically to be produced by RE cells. Thymic RE cells also produce numerous cytokines including IL-1, IL-6, G-CSF, M-CSF, and GM-CSF molecules that likely are important in various stages of thymocyte activation and differentiation. The co-existence of pituitary hormone and neuropeptide secretion [growth hormone (GH), prolactin (PRL), adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), triiodothyronine (T3), somatostatin, oxytocin (OT), follicle stimulating hormone (FSH), luteinizing hormone (LH), arginine vasopressin (AVP), growth hormone releasing hormone (GHRH), corticotropin releasing hormone (CRH), nerve growth factor (NGF), vasoactive intestinal peptide (VIP), pro-enkephalin (pro-enk), and beta-endorphin (beta-end)], as well as production of a number of interleukins and growth factors and expression of receptors for all, by RE cells is an unique molecular biological phenomenon. The thymic RE cell network is most probably comprised of cells organized into sub-networks--functional units composed of RE cells with differing hormone production/hormone receptor expression profiles, involved in the various stages of T lymphocyte maturation. Furthermore, it is quite possible that even on the level of individual RE cells, the numerous projections associated with a single cell, which engulf developing lymphocytes, nurturing and guiding them in their maturation, may differ in their hormone production and/or hormone receptor expression profile, thus allowing a single cell to be involved in distinct, separate steps of the T cell maturation process. Based on our systematic observations of the thymus in humans and other mammalian species, we suggest that the thymic RE cells represent an extremely important cellular and humoral network within the thymic microenvironment and are involved in the homeopathic regulation mechanisms of the multicellular organism, in addition to the presentation of various antigens to developing lymphocytes, and providing growth regulatory signals which may range from stimulatory to apoptotic signaling within the thymus. (ABSTRACT TRUNCA
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PMID:The role of the reticulo-epithelial (RE) cell network in the immuno-neuroendocrine regulation of intrathymic lymphopoiesis. 1092 21

Prostaglandin F2alpha (PGF2alpha) is a major physiological luteolysin in the cow. However, injection of PGF2alpha before day 5 (day 0 = estrus) of the estrous cycle dose not induce luteolysis. On the other hand, the early corpus luteum (CL) actively produces PGF2alpha. This indicates that luteal PGF2alpha may play a key role in the refractoriness to PGF2alpha injected during the early luteal phase when angiogenesis is active in the CL. Thus, this study aimed to investigate the possible interaction between pituitary hormones and local factors (luteal peptides) on secretion of PGF2alpha and progesterone (P) by the early bovine CL, and to evaluate the effect of growth hormone (GH) as well as its interactions on production of PGF2alpha in the developing CL. A RT-PCR analysis revealed that mRNA for GH receptor in CL was fully expressed from early in the luteal phase throughout the estrous cycle, while luteinizing hormone (LH) receptor mRNA was expressed less by the early and regressing CL than those at mid or late luteal phases (P < 0.05). For the stimulation test, an in vitro microdialysis system (MDS) was used as a model. Each bovine early CL (days 3-4) was implanted with the MDS, and maintained in an organ culture chamber. The infusion of GH, insulin-like growth factor-I (IGF-I) and oxytocin (OT) increased (P < 0.05) PGF2alpha and P release. In contrast, LH had no effect (P > 0.05) on PGF2alpha secretion and little effect on P release. Unexpectedly, there was no distinct interaction between pituitary hormones and luteal peptides on secretion of PGF2alpha and P. These results indicate that GH is a more powerful stimulator of PGF2alpha and P production in the early bovine CL than LH and suggest that GH and luteal peptides, IGF-1 and OT, contribute to maintenance of elevated PGF2alpha production in the developing bovine CL.
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PMID:Growth hormone, but not luteinizing hormone, acts with luteal peptides on prostaglandin F2alpha and progesterone secretion by bovine corpora lutea in vitro. 1120 40

Growth hormone secretagogues (GHSs) increase the activity of hypothalamic arcuate nucleus neurons thought to be involved in controlling the release of growth hormone (GH). The GHS receptor is also found in hypothalamic regions not associated with the release of GH, suggesting that GHSs may influence other hypothalamic systems. This study utilized double-labeling immunocytochemical techniques to examine the hypothalamic actions of a novel nonpeptide GHS, GHS-25. In common with other GHSs, GHS-25 induced significant amounts of Fos immunoreactivity in the arcuate nucleus of conscious male rats. However, unlike other GHSs, GHS-25 also induced Fos immunoreactivity in the supraoptic nucleus. Double labeling revealed that approx 66% of supraoptic nucleus cells that were Fos positive after the administration of GHS-25 were also immunoreactive for oxytocin. Thus, in addition to its actions on the GH axis, GHS-25 may influence the release of neurohypophyseal hormone.
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PMID:Central actions of the nonpeptide growth hormone secretagogue GHS-25. 1132 97

By use of an immunofluorescence histochemical technique with a cross-species reactive antiserum to porcine neurophysin-II the precise localization of neurophysin in the pituitary gland and the hypothalamic area of the brain of the sheep has been determined. Neurophysin was confined to neurosecretory pathways originating from the supraoptic and paraventricular hypothalamic nuclei. The major pathway terminates in the neurohypophysis but in addition a second neurophysin-containing pathway proceeds in the external infundibular zone of the median eminence-pituitary stalk and is associated with the presence of vasopressin. In sheep affected with the hereditary degenerative disease known as natural scrapie, this supraoptico-paraventriculo-infundibular pathway is preserved and hypertrophied, while the major pathway to the posterior lobe of the pituitary degenerates. The supraoptic and paraventricular nuclei in the sheep comprise at least two distinct but morphologically similar neuronal populations affected differently by the natural scrapie genome, one undergoing dissolution by middle-age and one surviving and becoming hyperactive. This premature ageing is probably associated with a primary biochemical lesion affecting the rate of the axonal flow of neurosecretory vesicles and of their discharge at synaptic terminals. Possible metabolic and circulatory bases for such an anomaly are considered. The presence of neurophysin in the rostral and caudal adenohypophysis supports the view that vasopressin is acting directly as a trophic-hormone releasing factor, possibly for the quick release of adrenocorticotropic hormone and of growth hormone. The relation of neurophysin-rich aggregations in the neurohypophysis to Herring bodies and the turnover of neurosecretory material are discussed.
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PMID:Neurophysin in the brain and pituitary gland of normal and scrapie-affected sheep--I. Its localization in the hypothalamus and neurohypophysis with particular reference to a new hypothalamic neurosecretory pathway to the median eminence. 1137 May 13

Vascular endothelial growth factor (VEGF) is the most important factor in the regulation of angiogenesis. Associated with luteinisation and formation of corpus luteum (CL) are alterations in luteal vascularity. The aim of the study was to test under in vitro conditions the stimulation of VEGF and progesterone (P) secretion of bovine granulosa cells by LH, IGF1 (insulin like growth factor) or by factors known to be produced by luteinised granulosa cells or in the early CL. Localisation of VEGF protein in preovulatory follicle and early CL were achieved by immunohistochemistry. LH and IGF1 stimulated dose dependently and significantly P and VEGF when tested alone. Both hormones added simultaneously had clear additive and even more interesting far greater (synergistic) effects on P with LH (0.1 ng/ml) plus 5 or 10 ng IGF1. In contrast, VEGF was stimulated only additively with 0.1 ng/ml of LH plus 5 or 10 ng IGF1. But with the higher dose of LH (1 ng/ml) additionally to the additive effect a tendency for a synergistic action (which was significant with 1 ng LH plus 5 ng IGF1/ml) was observed. Endothelin, oxytocin, progesterone, atrial natiuretic peptide, angiotensin II, prostaglandin F2 alpha alpha, prostaglandin E2, cortisol, fibroblast growth factor 1 and 2 and growth hormone showed no effect neither on P nor on VEGF. Tumour necrosis factor alpha (TNF alpha) stimulated (P < 0.05) VEGF with 10 or 100 ng/ml but not P. TPA (12-0 tetra decaenoyl-phorbol-13-acetate) or Ca2+ ionophore did not show a stimulatory effect in contrast to forskolin which increased P and VEGF secretion dose dependently. The VEGF protein was localised in follicle (granulosa cells, theca cells and some endothelial cells) and early (about 24 h after ovulation) CL (granulosa-lutein cells and endothelial cells). The same signalling pathway by stimulation of cAMP production and proteinkinase A activation for luteinisation and neo-vascularisation demonstrates a close temporal and spatial relationship of these normal physiological processes.
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PMID:Stimulatory and synergistic effects of luteinising hormone and insulin like growth factor 1 on the secretion of vascular endothelial growth factor and progesterone of cultured bovine granulosa cells. 1140 98

The effect of 10 peptides structurally related to the growth hormone (GH) releasing peptide hexarelin, injected into the paraventricular nucleus of the hypothalamus (PVN), on penile erection was studied in male rats. Six out of the 10 peptides tested induced penile erection in a dose-dependent manner. Among them, the most potent were EP 80661, EP 60761 and EP 91072, which were active at doses of 20-200 ng. The potency of these peptides in inducing penile erection is comparable to that of apomorphine, oxytocin and N-methyl-D-aspartic acid similarly injected into the PVN. Other peptides found active were EP 50885, EP 90101 and EP 91071, which induced penile erection at doses of 200-2000 ng. In contrast, EP 51322, EP 70555, EP 51216 and EP 91073 were inactive, as were hexarelin, EP 40904 and EP 40737 in a previous study. The majority of EP peptides found active when injected into the PVN induced penile erection, although to a lesser extent, also when given systemically (endovenously). The proerectile effect of EP peptides was prevented by the oxytocin receptor antagonist [d(CH2)5 Tyr(Me)2-Orn8]-vasotocin given into the lateral ventricles but not into the PVN, by the nitric oxide (NO) synthase inhibitor N(G)-nitro-1-arginine methyl ester given either into the lateral ventricles or into the PVN, by the N-type Ca2+ channel blocker omega-conotoxin GVIA and by morphine, but not by the dopamine receptor antagonist cis-flupenthixol or by the N-methyl-D-aspartic acid receptor antagonist dizolcipine, given into the PVN. As the structure-activity relationship of EP peptides for proerectile activity is different from those of other biological actions of these compounds, ie for GH release and eating behaviour, the present results suggest that EP peptides induce penile erection by acting on specific hypothalamic receptor sites that activate paraventricular oxytocinergic neurons projecting to extrahypothalamic brain areas that mediate this sexual function by a mechanism similar to that of dopamine receptor agonists, oxytocin and N-methyl-D-aspartic acid.
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PMID:EP 60761- and EP 50885-induced penile erection: structure-activity studies and comparison with apomorphine, oxytocin and N-methyl-D-aspartic acid. 1142 62

The effect of EP 91073, EP 51389, EP 70555 and EP 51216, peptide analogues of the growth hormone releasing peptide hexarelin, on penile erection induced by EP 80661 or EP 60761 injected into the paraventricular nucleus of the hypothalamus, was studied in male rats. Of the above peptides only EP 91073 (0.2-1 microg) was found capable of reducing penile erection induced by EP 80661 or EP 60761, when given into the paraventricular nucleus. Despite its ability to prevent EP peptide-induced penile erection, EP 91073 (1 microg) was unable to prevent penile erection induced by the dopamine receptor agonist apomorphine (50 ng), oxytocin (30 ng) and N-methyl-D-aspartic acid (50 ng), when given into the paraventricular nucleus 10 min prior to the above substances. The EP 91073-induced prevention of penile erection occurred with a reduction in the increase in nitric oxide production that occurs in the paraventricular nucleus concomitant to penile erection induced by EP 80661 and EP 60761, as measured by intracerebral vertical microdialysis. The present results are in line with the hypothesis that EP 80661 and EP 60761 induce penile erection by activating specific receptors in the paraventricular nucleus, located possibly in oxytocinergic neurons mediating penile erection, and show that EP 91073 acts as an antagonist of these EP peptide receptors mediating penile erection.
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PMID:EP 91073 prevents EP 80661-induced penile erection: new evidence for the existence of specific EP peptide receptors mediating penile erection. 1148 62

The action of growth hormone (GH) on the production of hormones, growth factors, growth factor binding protein and the occurrence of apoptosis in porcine ovarian granulosa cells, as well as the role of cAMP-stimulated protein kinase A (PKA) in the mediation of these effects, were studied. For this purpose, the effects of exogenous pGH (1-10,000 ng/ml), PKA blockers KT5720 (100 ng/ml) and Rp-cAMPS (1micromol), alone and in combination, on insulin-like growth factor type I (IGF-I), insulin-like binding protein 3 (IGFBP-3), oxytocin (OT) and prostaglandin F alpha (PGF) secretion, PKA and cAMP response element binding transcription factor (CREB) content and the occurrence of apoptosis were investigated. It was found (using RIA/IRMA) that GH addition to culture medium significantly stimulated IGF-I and PGF release and inhibited IGFBP-3 and OT secretion. GH significantly decreased the incidence of apoptosis (TUNEL method) in cultured cells. Immunocytochemical study and Western immunoblotting showed, that addition of GH caused a dramatic increase in the accumulation of immunoreactive PKA within the cells, whilst Western blotting did not reveal marked influence of GH on content of CREB in cell lysates. PKA blockers, given alone, were able to decrease IGFBP-3 output (Rp-cAMPS, but not KT5720), reduce basal OT release (either Rp-cAMPS and KT5720) and increase PGF accumulation (KT5720, but not Rp-cAMPS). Furthermore, PKA blockers were able to prevent stimulatory effects of GH on IGF-I and PGF release, and inhibitory effect of GH on IGFBP-3, OT output and on apoptosis. These observations suggest the involvement of GH and a PKA-dependent intracellular mechanism in the control of IGF-I, IGFBP-3, OT, PGF, cAMP and apoptosis in porcine ovarian granulosa cells. Stimulation of PKA by GH and the prevention of GH-induced effects by PKA blockers suggest that both stimulatory and inhibitory effects of GH on porcine ovarian cells are probably mediated by the cAMP/PKA system.
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PMID:Growth hormone can regulate functions of porcine ovarian granulosa cells through the cAMP/protein kinase A system. 1184 11

The pituitary gland, the "master gland" of the body, is composed of endocrine cells, which secrete hormones essential for homeostasis. The gland consists of the adenohypophysis (anterior pituitary) and the neurohypophysis (posterior pituitary), two unique structures that differ anatomically and functionally. The neurohypophysis is innervated by nerve cells in the hypothalamus and forms the connection between it and the pituitary gland. The hypothalamus stimulates release and inhibition of pituitary hormones. The neurohypophysis secretes oxytocin and antidiuretic hormone. The adenohypophysis is composed of three structures: the pars distalis, the pars intermedia, and the pars tuberalis. The anterior pituitary (pars distalis) is responsible for the release of hormones that include growth hormone, prolactin, thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone, adrenocorticotropic hormone, and melanocyte-stimulating hormone. Disorders of the pituitary are predominately those of insufficient hormone release and may have profound effects on the neonate. The potential causes of and clinical symptomatology that may accompany pituitary hormone insufficiency in the neonatal period are explored.
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PMID:The pituitary gland: embryology, physiology, and pathophysiology. 1194 4


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