Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progestin receptor-containing cells in the hypothalamus of the adult female green monkey (Cercopithecus aethiops) were examined by double-label immunocytochemical methods to determine their anatomical location, neurotransmitter content and afferent connections. Animals were ovariectomized and administered either estradiol valerate or the oil injection vehicle, and were sacrificed after 10 days of treatment. Using a monoclonal antibody raised against rabbit uterine progestin receptor (PR), the distribution of PR-immunoreactive cells in the mediobasal hypothalamus and the effect of estrogen treatment on this distribution was determined. PR-immunoreactive cells were found throughout the ventromedial nucleus (VMN), in the area between the VMN and fornix, and in the medial portion of the infundibular nucleus. Estrogen treatment dramatically increased both the number of labeled cells and the intensity of immunoreaction product in these regions. In double-immunostained sections, boutons immunoreactive for antigens indicative of serotonin, pro-opiomelanocortin derived peptides, GABA, catecholamine, neuropeptide Y, substance P, cholecystokinin, and somatostatin were demonstrated to establish synaptic contact with the soma of PR-immunoreactive hypothalamic neurons. In colchicine-pretreated animals, all PR-containing neurons in the mediobasal hypothalamus were found to contain immunoreactivity for glutamic acid decarboxylase, the enzyme required for synthesis of GABA. No evidence of colocalization with other antigens, including LHRH, was observed. Because LHRH neurons are known to receive a rich GABAergic innervation PR-containing GABAergic cells may represent steroid-sensitive sites of integration for inputs from other neural systems involved in the control of gonadotropin secretion.
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PMID:Transmitter content and afferent connections of estrogen-sensitive progestin receptor-containing neurons in the primate hypothalamus. 135 61

The presence of progesterone, oestrogen, somatostatin and epidermal growth factor receptors of 24 meningiomas was related with their radiological CT appearance. Progesterone receptors were present in 16 of 21 (76%), oestrogen receptors in 4 of 21 (19%), somatostatin receptors on 23 of 24 (96%) and epidermal growth factor receptors on 17 of 19 (89%) meningiomas. There was no relationship between the presence of these receptors and the age or sex of the patients, tumour histology, tumour localisation, the presence of perifocal oedema, displacement of the midline cerebri or obstructive hydrocephalus on CT scan. There was a negative correlation (P less than 0.05) between the number of progesterone receptors and "malignant" behaviour of the meningiomas on CT (e.g. the presence of necrosis, cyst formation, intratumoral haemorrhage, irregular surface and/or inhomogeneous attenuation of contrast). The observation that aggressive tumour behaviour on CT is accompanied by low numbers or absence of progesterone receptors makes these meningiomas less attractive candidates for medical therapy with antiprogestins.
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PMID:Progesterone, oestradiol, somatostatin and epidermal growth factor receptors on human meningiomas and their CT characteristics. 166 Feb 95

The modulatory effects of glucocorticoid and sex steroid hormones on the effects of rat GH-releasing factor (GRF) and somatostatin (SRIF) on GH release and biosynthesis were studied in monolayer cultures of rat anterior pituitary cells with RIA and quantitative immunoprecipitation methods. Dexamethasone (10(-7) M), a potent synthetic glucocorticoid, increased both the sensitivity and maximum response of GH release stimulated by GRF. Progesterone (10(-7) M) also enhanced GH release stimulated by GRF. The stimulatory effects of dexamethasone and progesterone were dose dependent and required a latent period of at least 24 h to be evident. Testosterone, dihydrotestosterone, and 17 beta-estradiol showed no apparent influence on GRF-induced GH release under the same conditions. None of the hormones studied showed significant influences on basal or SRIF-suppressed GH release. Progesterone added to the maximally effective concentrations of dexamethasone had no additional effects on GRF-induced GH release. The effect of progesterone was attenuated by both 5 alpha-dihydronorethindrone, a progesterone antagonist and 17 alpha-methyltestosterone, a glucocorticoid antagonist. In terms of GH synthesis, stimulatory effects of GRF on GH synthesis were apparent only when pituitary cells were pretreated with dexamethasone. These results indicate that: pretreatment with glucocorticoid or progesterone enhances the effects of GRF on GH release and/or synthesis; these two steroids share at least one common step to enhance GRF effects; and steroid hormones have little influence on basal or SRIF-suppressed GH release.
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PMID:Influence of sex steroid hormones on rat growth hormone-releasing factor and somatostatin in dispersed pituitary cells. 287 86

In contrast to the protective, anti-proliferative, action of progestins on the development of endometrium cancer, progestins may have local stimulatory and inhibitory effects on the proliferation of mammary epithelium. Until now there was no final molecular explanation of this discrepancy. Prolonged treatment of dogs with depot medroxyprogesterone acetate (DPMA) or with proligestone (PROL) results in enhanced plasma concentrations of growth hormone (GH), insulin-like growth factor (IGF)-I, IGF-II and IGF-binding proteins, together with the development of benign mammary tumours. The stimulated plasma GH levels do not have the typical pulsatile secretion pattern, and are not sensitive to stimulation with GHRH or to inhibition with somatostatin. The autonomous secretion can be inhibited by the anti-progestin RUU-486. The source of progestin-induced plasma GH levels has been demonstrated to be the canine mammary gland where progestins induce the expression of the gene encoding GH. The expression of the GH gene is restricted to focal areas of hyperplastic epithelium as shown by immunohistochemistry, and is predominantly located in single positive epithelial cells with an intermediate position between luminal- and myo-epithelium. Progestin-induced fibroadenomatous changes in the mammary gland of cats are also associated with locally enhanced GH expression. In both normal, benign and malignant mammary tumours of humans GH mRNA expression has been demonstrated by RT-PCR. The presence of GH mRNA is associated with the presence of immunoreactive GH as shown by immunohistochemistry. Sequence analysis revealed 100% homology to the pituitary expressed GH gene. In malignant mammary tumours of humans and dogs GH expression is also found in specimens negative for progesterone receptors as measured by ligand binding. It is concluded that the gene encoding GH is expressed in the mammary gland of a variety of species, including man. This appears to represent a contribution to the molecular explanation of the action of progestins on proliferation of mammary epithelium. It needs, however, to be proven whether this local biosynthesis of GH in the mammary gland is the cause of the local stimulatory effect of progestins on the proliferation of mammary epithelium.
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PMID:New insights in the molecular mechanism of progestin-induced proliferation of mammary epithelium: induction of the local biosynthesis of growth hormone (GH) in the mammary glands of dogs, cats and humans. 864 18

Progesterone plays an important role in regulating reproductive behaviour in guinea-pigs through actions exerted at the ventrolateral nucleus (VL), an area of the brain that contains progesterone receptors (PR) and neuroactive peptides, somatostatin (SOM), neurotensin (NT) and substance P (SP). Previous double-label analyses provided evidence that a substantial proportion of these neuropeptidergic cells contain PR. By means of triple-label immunofluorescence histochemistry, we examined whether PR are colocalized with two neuropeptides (SOM + NT or SP + SOM or SP + NT) within the same neurons in the VL. Ovariectomized guinea-pigs were primed with estradiol to induce PR immunoreactivity, and treated with colchicine to visualize immunoreactive (IR) neuropeptidergic cells. Both monoclonal mouse PR and polyclonal rabbit neuropeptide antibodies were used in double staining and in elution-restaining experiments. In the whole VL, the proportion of each coexisting peptide with PR obtained after double immunofluorescence appeared in decreasing order as: SOM (34%)>NT (25%)>SP (20%). Occasional colocalization was seen between PR and two neuropeptides throughout the rostrocaudal extent of the VL. Combining our various quantitative observations, we found that, of the total population of PR-IR neurons containing any combination of SOM, NT and SP, only about 1.5% contained SOM and NT, 2% contained SP and SOM and 1.6% contained SP and NT. These results indicate that while many PR-IR neurons also contain SOM or NT or SP in the guinea-pig VL, there may be very few PR-IR neurons that express more than one of these three peptides.
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PMID:Multiple peptides infrequently coexist in progesterone receptor-containing neurons in the ventrolateral hypothalamic nucleus of the guinea-pig: an immunocytochemical triple-label analysis of somatostatin, neurotensin and substance P. 957 4

A number of hormones, including hypothalamic neuropeptides acting as neurotransmitters and neuromodulators in the CNS, are involved in the physiologic regulation of breathing and participate in adjustment of breathing in disease. In addition to central effects, some hormones also control breathing at peripheral chemoreceptors or have local effects on the lungs and airways. Estrogen and progesterone seem to protect from sleep-disordered breathing, whereas testosterone may predispose to it. Progesterone and thyroxine have long been known to stimulate respiration. More recently, several hormones such as corticotropin-releasing hormone and leptin have been suggested to act as respiratory stimulants. Somatostatin, dopamine, and neuropeptide Y have a depressing effect on breathing. Animal models and experimental human studies suggest that also many other hormones may be involved in respiratory control.
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PMID:Hormones and breathing. 1247 61