Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-1 (IL-1) has been suggested to directly affect pituitary growth hormone (GH) release, although other investigators have failed to observe this effect. We examined the effects of IL-1 beta on GH secretion from single somatotrophs by means of reverse hemolytic plaque assay (RHPA). Anterior pituitary cells of adult male rats were enzymatically dispersed and subjected to RHPA. IL-1 beta at 100 pM and 1 nM, increased both the mean plaque area and the fraction of somatotrophs forming large plaques. IL-1 beta did not increase the mean plaque area in the presence of the IL-1 receptor antagonist (IL-1ra). IL-1 beta (1 nM) added together with GH-releasing hormone (GHRH; 10 nM), showed no additive effect on GHRH-induced GH release. The stimulatory action of IL-1 beta on the release of GH was suppressed by somatostatin. In conclusion, our data show that IL-1 beta stimulates GH-secretion through direct action on the pituitary.
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PMID:Analysis of growth hormone release from rat anterior pituitary cells by reverse hemolytic plaque assay: influence of interleukin-1. 796 61

Recent findings indicate that excitatory amino acids (EAAs) can modulate growth hormone (GH) secretion in several mammalian species in vivo and in vitro. In this study, we examined the effects of EAA receptor antagonists [N-methyl-D,L-aspartate (NMDA), kainic acid, L-glutamate] on GH secretion by the reverse hemolytic plaque assay (RHPA). Anterior pituitary cells of adult male Sprague-Dawley rats were enzymatically dispersed and subjected to RHPA. EAA receptor agonists increased the mean plaque area in a dose-dependent manner: the maximal increase was observed at 10 microM and increased the fraction of somatotrophs forming large plaques. NMDA (10 microM) did not increase the mean plaque area in the presence of the NMDA receptor antagonists 10 microM AP-7 and 10 microM MK-801. Coincubation of kainic acid with the non-NMDA receptor antagonist CNQX blocked the kainic-acid-stimulated increase in GH secretion. The addition of MK-801, AP-7 or CNQX to glutamate caused a partial reduction of the mean plaque area. Ten micromoles per liter glutamate with 10 nM GH-releasing hormone (GHRH) produced an additive effect on GHRH-induced GH release. Somatostatin suppressed the stimulatory action of glutamate. We speculate that glutamate plays a role in the regulation of GH secretion.
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PMID:Effect of excitatory amino acid receptor agonists on secretion of growth hormone as assessed by the reverse hemolytic plaque assay. 796 75

As part of an ongoing investigation devoted to understanding the pathogenesis of senile plaques, we employed histochemical and immunocytochemical techniques to examine the distribution and cytologic features of acetylcholinesterase (AChE), choline acetyltransferase (ChAT), somatostatin (SOM), neurotensin (NT) and substance P (SP) containing fibers and neurons within the amygdala of: (1) patients with Alzheimer's disease (AD); (2) age-matched non-demented controls (NC); and (3) a group of non-demented cases, who upon postmortem neuropathologic examination exhibited sufficient numbers of senile plaques to be classified as AD. This latter group was referred to as high plaque non-demented (HPND). For every case, the distribution of immunolabeled fibers and neurons were determined for each transmitter throughout the various subnuclei of the amygdala. In addition, in the AD and HPND cases the topographic distribution of senile plaques was determined throughout the amygdala using thioflavine-S and Bielschowsky silver methods. In the amygdala, the distribution and density of senile plaques were not bound by conventional cytoarchitectural groupings but rather were most dense in the ventromedial regions of the amygdala with decreasing density in dorsal and lateral directions. Importantly, the density and distribution of senile plaques failed to correlate with the normal topography and/or density of the various peptidergic or cholinergic fibers within the amygdala. The finding that plaques do not correlate with the topographic distribution of any specific transmitter system suggests that plaques likely do not arise from the degeneration of a single neurotransmitter system (i.e., the cholinergic system). However, the finding that in AD a transmitter is most markedly depleted in regions of greatest plaque density, suggests certain constituents of the plaque (e.g. beta-amyloid) may be contributing to the degeneration of local fibers. The extent to which a transmitter was depleted in AD patients varied considerably among those four investigated with the cholinergic and NT systems displaying the most dramatic reductions, followed by SP and SOM. Despite these differential reductions in fiber density, all four neurotransmitters were found localized within dystrophic neurites and in most instances these dystrophic neurites were associated with thioflavine-positive senile plaques. In contrast to the AD cases, the HPND cases were characterized by no significant reductions in immunolabeled fibers, although immunostained dystrophic neurites were very prevalent in the HPND cases. These data suggest that dystrophic neurites occur very early in the disease process and likely precede the actual loss of fibers when or if it occurs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunocytochemical distribution of peptidergic and cholinergic fibers in the human amygdala: their depletion in Alzheimer's disease and morphologic alteration in non-demented elderly with numerous senile plaques. 824 91

Previous in vivo studies demonstrated that estrogen treatment of male rats allows somatostatin (SRIF) to inhibit PRL release. The objective of this study was to determine whether chronic estrogen (E2) treatment of male rats can induce the conversion of somatotropes to mammosomatotropes. In situ hybridization and reverse hemolytic plaque assay were used to evaluate the effects of E2 treatment on GH and PRL messenger RNA (mRNA) content and hormone secretion in individual pituitary cells. Male rats were implanted for 2-6 weeks with placebo or estradiol-containing pellets (5mg/90-day release). Pituitaries were removed and prepared for reverse haemolytic plaque assay to determine PRL and GH secretion. This was followed by in situ hybridization using 35S-labeled riboprobes for PRL and GH mRNA. Chronic E2 treatment increased both the percentage of pituitary cells that secreted PRL and the amount of PRL secreted per cell. Concomitantly, there was a decrease in both the percentage of GH-secreting cells and that amount of GH secreted per cell. In situ hybridization demonstrated that E2 treatment increased PRL mRNA while decreasing GH mRNA in single pituitary cells. Significantly, in control male rat pituitary cell cultures, no PRL-secreting cells were positive for GH mRNA. In contrast, after chronic E2 treatment, 10% of PRL-secreting cells contained GH mRNA. In the control pituitary cell cultures, SRIF had no effect on PRL release, but SRIF significantly inhibited PRL release from pituitary cell cultures prepared from E2-treated male rats. These studies demonstrate that the adult pituitary preserves plasticity and, under the appropriate steroid milieu, allows conversion of somatotropes to mammosomatotropes.
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PMID:Chronic estrogen treatment in male rats reveals mammosomatotropes and allows inhibition of prolactin secretion by somatostatin. 853 23

Immunosuppressant agent FK506 has been reported to stimulate ACTH release from pituitary cells. We examined the effects of FK506 on GH release from the rat anterior pituitary cells and the effects of FK506 on hypothalamic GH- releasing hormone (GRH) and somatostatin (SS) gene expression in conscious male rats. In vitro experiments, the monolayer pituitary culture and reverse hemolytic plaque assay were employed to examine the GH release from the rat anterior pituitary cells. In in vivo experiments, the FK506 was administered for 7 days and then sequential blood sampling was performed every 20 min during 6 h in conscious rats. The hypothalamus was removed, and total RNA was extracted for Northern blot analysis. The FK506 significantly stimulated GH release from the rat anterior pituitary cells in a dose-dependent manner in vitro. In in vivo experiments, the area under the curve of GH surges was significantly increased in FK506-treated rats, although the peak height and the trough level of GH surges were not altered. Pituitary GH messenger RNA (mRNA) levels were significantly increased by the FK506 treatment. Hypothalamic GRH mRNA levels were significantly increased in FK506- treated rats, whereas hypothalamic SS mRNA levels were not altered. These findings indicate that FK506 stimulates GH secretion and gene expression of hypothalamic GRH in the rat.
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PMID:Immunosuppressant agent FK506 stimulates growth hormone (GH) secretion and gene expression of hypothalamic GH-releasing hormone in the rat. 860 82

Primary culture of rat islets of Langerhans lose glucose responsiveness and eventually die when cultured for a long period of time. In this study we evaluated the effect of matrigel, a basement membrane extract, on (i) islet cell survival, (ii) cell responsiveness following a glucose challenge, and (iii) mRNA levels for insulin, glucagon, and somatostatin. Pancreatic islets were isolated by collagenase digestion and plated in culture dishes either coated or not with a matrigel layer. Using the reverse hemolytic plaque assay, we determined the total number of insulin-secreting cells and the amount of insulin secreted by individual beta cells. After 1 h of exposure to 5 mM glucose, beta cells from 6-month-old rat islets cultured for 6 weeks on matrigel showed an equal number of insulin-secreting cells compared to freshly isolated islets cultured for only 3 days in the absence of matrigel (39.5 +/- 2.5 vs. 37.1 +/- 2.6%). Furthermore, the release of insulin by cells cultured on matrigel for 6 weeks increased in a glucose-dependent manner (p < 0.001) and showed an ED50 of 7 mM. However, the amount of insulin released per single beta cell was reduced by 40-60% (p < 0.02) compared to that released from isolated beta cells derived from a 3-day culture of islets. Finally, there was a 35-55% increase (p < 0.05) in the levels of insulin, glucagon, and somatostatin mRNAs in cells cultured for 6 weeks on matrigel. These data suggest a trophic effect of matrigel on the maintenance of normal beta-cell activity and function and may lead the way to the development of a new model for the study of pancreatic islets in long-term culture.
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PMID:Insulin release and insulin mRNA levels in rat islets of Langerhans cultured on extracellular matrix. 878 33

Dwarf tyrosine hydroxylase-human GH (TH-hGH) transgenic mice carrying the hGH reporter gene targeted by the TH promoter express hGH in those regions of the hypothalamus responsible for regulation of pituitary GH secretion. Central expression of the hGH gene decreases GH-releasing hormone (GHRH) and increases somatostatin, which ultimately impacts on pituitary function by reducing the overall amount of GH produced. In the present study, we sought to determine if the reduction of pituitary GH in TH-hGH mice could be attributed to a decrease in somatotrope cell numbers and/or an impairment of somatotrope function. Pituitaries from TH-hGH or wild-type (WT) male and female mice were enzymatically dispersed, counted, and immunostained for GH, PRL, TSH, and ACTH. The total number of pituitary cells recovered from TH-hGH pituitaries was approximately one-half of that from WT controls. However, the proportion of cells that stained for GH and PRL were virtually identical (males, GH-TH-hGH, 58.1 +/- 1.0% [mean +/- SEM] vs. WT, 60.7 +/- 1.0%; PRL-TH-hGH, 43.4 +/- 2.2% vs. WT, 43.1 +/- 0.7%; females, GH-TH-hGH, 47.9 +/- 2.3% vs. WT, 41.5 +/- 3.5%; PRL-TH-hGH, 43.3 +/- 3.2% vs. WT, 47.1 +/- 3.3%). In contrast, percentages of both TSH- and ACTH-containing cells were increased in TH-hGH pituitaries relative to controls (males, TSH-TH-hGH, 15.1 +/- 2.3% vs. WT, 9.6 +/- 1.5%; ACTH-TH-hGH, 24.5 +/- 2.5% vs. WT, 10.9 +/- 0.9%; females: TSH-TH-hGH, 11.3 +/- 0.7% vs. WT, 7.5 +/- 0.6%; ACTH-TH-hGH, 19.8 +/- 1.6% vs. WT, 9.3 +/- 0.8%; P < 0.05). Calculation of the absolute number of each cell type per pituitary demonstrated TH-hGH mice to have about one-half the number of GH and PRL cells, whereas TSH and ACTH cell populations were comparable with that of their WT counterparts. Immunocytochemical localization of GH cells within pituitary sections from TH-hGH mice revealed that somatotropes were confined primarily to the lateral wings of the adenohypophysis, in contrast to the heterogeneous distribution of GH-immunostained cells in WT pituitaries. To assess the functional capacity of the somatotrope populations, pituitary cells from TH-hGH and WT mice were challenged with mouse GHRH (0.01-10 nM). The quantity of GH released (as assessed by both RIA and reverse hemolytic plaque assay) under basal and stimulated conditions did not differ among TH-hGH and WT pituitary cell cultures. Similarly, GHRH induced intracellular cAMP levels were comparable. These results indicate that proliferation of pituitary somatotropes and lactotropes is much more sensitive to changes in GHRH input than is the capability of developing regulated GH secretory function.
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PMID:The tyrosine hydroxylase-human growth hormone (GH) transgenic mouse as a model of hypothalamic GH deficiency: growth retardation is the result of a selective reduction in somatotrope numbers despite normal somatotrope function. 889 26

The synthetic hexapeptide GH-releasing peptide (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2; GHRP-6) and GH releasing hormone (GHRH) are both potent stimulators of GH release in rats. Using reverse hemolytic plaque assay (RHPA), we have compared the effects of human GHRH and GHRP-6 on GH release from the dispersed individual cells of rat anterior pituitary. In a single RHPA, we quantified the percentage of plaque forming cells (% PFC) and their mean plaque area (MPA) after 30 min-incubation, and calculated a total secretion index (TSI) by multiplying % PFC and MPA. 10 nM GHRH and 100 nM GHRP-6 each caused a significant increase in % PFC (%) (GHRH 39.15, GHRP-6 29.4, vs vehicle 24.3, P < 0.01), MPA (x 10(-2) microns2) (GHRH 124.04, GHRP-6 94.80, vs vehicle 44.57, P < 0.01) and TSI (x 10(-2)) (GHRP-6 32.87, vs vehicle 10.84, P < 0.01). Simultaneous addition of both secretagogues caused a further increase in GH release (%PFC 46.4, MPA 142.55, TSI 69.82, P < 0.01 vs vehicle), although the effect was additive but not synergistic. Somatostatin analog, SMS201-995 (SMS) partially suppressed all parameters in GH secretion after stimulation by GHRH and/or GHRP-6. A double RHPA was then performed to test whether all somatotrophs respond equally to GHRH and GHRP-6 or some cells formed plaques only be either GHRH or GHRP-6. There were somatotrophs responsive to only GHRH (23.3% vs control 6.2%, P < 0.01), those responsive to only GHRP-6 (11.9% vs control 6.1%, P < 0.01), and those responsive to both GHRH and GHRP-6 (7.8% vs control 0.2%, P < 0.01). These results confirmed the previous findings that GHRP-6 and GHRH directly but independently stimulate GH release from the pituitary cells, and further suggest that presence of at least three functionally distinct somatotroph subpopulations concerning the responsiveness to GHRP-6 and GHRH in rats.
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PMID:Growth hormone (GH)-releasing peptide and GH releasing hormone stimulate GH release from subpopulations of somatotrophs in rats. 893 59

The present study was designed to investigate the modulating effect of aging and lifelong dietary restriction (DR), a powerful anti-aging intervention in laboratory rodents, on growth hormone (GH) secretion from pituitary cells in response to GH-releasing hormone (GHRH) in the presence of somatostatin (SS)-28. Dispersed pituitary cells from 6- and 24-month-old rats fed ad libitum (AL-Y, AL-O, respectively) and 24-month-old rats dietary restricted from 6 weeks of age (DR-O) were subjected to a reverse hemolytic plaque assay under variable conditions including GHRH (0, 1, 10 nM) and SS-28 (0, 10 nM). The proportion of GH plaque-forming cells in dispersed pituitary cells increased by GHRH and decreased by SS-28. The proportion of these cells was lowest in AL-O rats; it was lower in DR-O than in AL-Y rats, particularly in the presence of SS-28. The reduction in these cells by SS-28 was greatest in Group AL-O. The mean area of these plaques, reflecting the amount of GH released from individual cells, was not different among the three rat groups in the absence of SS-28. In contrast, SS-28 produced a significantly higher reduction in the plaque area in Group AL-O compared with AL-Y and DR-O rats. Our results indicated that: (1) aging did not alter the responsiveness of GH-secreting cells to GHRH for GH secretion, while increased sensitivity of GH-secreting cells to SS-28 was noted in aged rats; (2) lifelong dietary restriction did not modulate the responsiveness to GHRH but partially inhibited the age-related increase in the sensitivity to SS-28 of GH-secreting cells, and (3) the major impact of the dietary regimen may include modulation of the number of pituitary cells, which leads to a high proportion of GH-secreting cells compared with that in AL rats at the same chronological age.
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PMID:Effect of somatostatin-28 on growth hormone response to growth hormone-releasing hormone--impact of aging and lifelong dietary restriction. 915 69

We have previously demonstrated that chicken embryonic somatotropes are responsive to GHRH shortly after they differentiate. In contrast, relatively little is known about the regulation of GH secretion by somatostatin (SRIF) and IGF-I during chicken embryonic development. In the present study, anterior pituitary cells were isolated from day. 16, 18 and 20 embryos and subjected to reverse hemolytic plaque assays (RHPAs) for chicken GH to assess the effect of SRIF and IGF-I on basal GH release and SRIF on GHRH-stimulated GH secretion. We found that all three ages responded to SRIF, under both basal and stimulated conditions. SRIF inhibition of basal GH release was evident for day 18 and 20 cells by 9 h, while 18 h were required for day 16 cells. After 18 h, 10(-11) M SRIF depressed basal GH secretion by day 16 and 18 cells, while 10(-9) M SRIF was required to depress GH plaque percentages by day 20 cells. GHRH stimulated GH release from all ages tested. After 2 h, SRIF partially suppressed GHRH-stimulated GH release by day 20 cells. After 6 h, day 18 cells responded to SRIF, reducing the percentage of plaque-forming cells under GHRH stimulated conditions. After 18 h, the percentage of day 16 cells forming GH plaques was reduced for cells treated with GHRH and SRIF, compared with cells treated with GHRH alone. All ages examined also responded to IGF-I. After 36 h, GH release by day 16 and 18 cells was decreased when exposed to IGF-I. While IGF-I decreased the relative amount of GH secreted per somatotrope on day 20, a paradoxical increase in the percentage of cells secreting GH was noted. These results indicate that anterior pituitary somatotropes are responsive to SRIF and IGF-I during late embryonic development of chickens.
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PMID:Responsiveness of chicken embryonic somatotropes to somatostatin (SRIF) and IGF-I. 929 41


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