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)

Porcine vasoactive intestinal peptide stimulated adenosine 3':5'-monophosphate (cyclic AMP) production in rat intestinal epithelial cells. The stimulation was dependent on time and temperature and was potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Under optimal conditions (at 15 degrees C, with 0.2 mM 3-isobutyl-1-methylaxanthine, at a cell concentration up to 18 microgram DNA/ml), the cyclic AMP production produced by vasoactive intestinal peptide was constant for 10 min and stopped after 15 min incubation, at either low (1 nM) or high (30 nM) concentration of the peptide. This plateau effect was demonstrated not to be due to an inactivation of vasoactive intestinal peptide in the medium nor to an alteration of receptors for the peptide. Cyclic AMP production was sensitive to a concentration as low as 0.1 nM vasoactive intestinal peptide. Maximal stimulation of cyclic AMP levels by vasoactive intestinal peptide was observed with 30 nM vasoactive intestinal peptide and represented an 11-fold increased above basal. The dorse-response curve was monophasic with a Km of 2.3 x 10(-9) M. No cooperative effects were detected by Hill analysis. The positive non-linear relationship observed between stimulation of cyclic AMP production and occupancy of binding site was not time-dependent as indicated by experiments performed after 15, 45 and 120 min incubation. Maximal and half-maximal responses were obtained at about 70% and 7% occupation of binding sites, respectively. Chicken vasoactive intestinal peptide and porcine secretin were agonists of porcine vasoactive intestinal peptide with a 6-times and a 120-times lower potency, respectively. Among secretin analogs that were found to have low affinity for vasoactive intestinal peptide binding sites, [4-alanine, 5-valine]secretin, that resembles vasoactive intestinal peptide at the first seven amino acids at the N-terminal end, was a partial agonist of vasoactive peptide at the first seven amino acids at the N-terminal end, was a partial agonist of vasoactive intestinal peptide and others failed to stimulate cyclic AMP production. Glucagon (10microM), gastric inhibitory peptide (0.1 microM), substance, P, neurotensin, octapeptide of cholecystokinin, bovine pancreatic polypeptide, human gastrin I with leucine at residue 15, Leu-enkephalinand somatostatin (1 microM) did not alter cyclicAMP levels. Non-peptide mediators such as dopamine, serotonin, acetylcholine and histamine, tested at 10 microM, were also ineffective. Prostaglandins E2, E1 and isoproterenol, tested at 10 microM, induced an increase of cyclic AMP levels above basal but were 9.5, 13.7 and 17.5 times less efficient than vasoactive intestinal peptide, respectively. Thus vasoactive intestinal peptide is a unique stimulus of cyclic AMP production in rat intestinal epithelial cells.
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PMID:Interaction of vasoactive intestinal peptide with isolated intestinal epithelial cells from rat. 2. Characterization and structural requirements of the stimulatory effect of vasoactive intestinal peptide on production of adenosine 3':5'-monophosphate. 8 68

DNA sequences corresponding to specific genes may be prepared by chemical synthesis, isolation of naturally occurring DNA, or reverse transcription. Such DNA may then be inserted into vectors such as plasmids or bacteriophages which carry the DNA into bacterial cells. Although significant differences exist in the basic molecular biology of eucaryotic and procaryotic organisms, these differences do not constitute absolute barriers to the expression of eucaryotic genes in bacteria. Several eucaryotic proteins, including insulin, growth hormone, ovalbumin, dihydrofolate reductase and somatostatin have been produced in bacteria. The use of chimeric microorganisms harboring recombinant DNA offers a completely new approach to the production of biologically useful polypeptides.
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PMID:Use of recombinant DNA technology for the production of polypeptides. 9 11

The role of gastrointestinal and pancreatic hormones in regulating liver growth was evaluated by measuring their effect on DNA synthesis in the normal and regenerating liver of rats in vivo and in maintenance cultures of adult rat hepatocytes in vitro. After partial liver resection DNA synthesis reached peak levels after 24 hours while serum concentrations of immunoreactive insulin in portal and peripheral blood at this time were still suppressed. Increase of endogenous insulin levels by intravenous glucose infusion or portal infusion of insulin, glucagon or both together with glucose did not change DNA synthesis in normal or regenerating rat liver. After acute carbon tetrachloride poisoning of rats, survival rate and degree of liver necrosis was not changed by intraperitoneal infusion of glucagon and insulin with glucose. In vitro, insulin, glucagon and somatostatin synergistically stimulated the specific thymidine uptake in seven-day-old maintenance cultures of rat hepatocytes. The hormones did not cause cell multiplication but enhanced cell survival, probably by improving the uptake and utilization of nutrients. Gastrin G-17, secretin and cholecystokinin (contaminated with gastric inhibitory polypeptide) had no effect. It is concluded that the results do not support the contention that liver regeneration is regulated by the known pancreatic hormones. However, a trophic effect of pancreatic hormones on liver cells in vitro could be demonstrated. Gastrointestinal hormones had no such effect.
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PMID:Hepatotrophic effects of pancreatic and gastrointestinal hormones in the rat in vivo and in vitro. 24 3

A gene for somatostatin, a mammalian peptide (14 amino acid residues) hormone, was synthesized by chemical methods. This gene was fused to the Escherichia coli beta-galactosidase gene on the plasmid pBR322. Transformation of E. coli with the chimeric plasmid DNA led to the synthesis of a polypeptide including the sequence of amino acids corresponding to somatostatin. In vitro, active somatostatin was specifically cleaved from the large chimeric protein by treatment with cyanogen bromide. This represents the first synthesis of a functional polypeptide product from a gene of chemically synthesized origin.
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PMID:Expression in Escherichia coli of a chemically synthesized gene for the hormone somatostatin. 41 51

The effect of maternal somatostatin administration from days 14 to 20 of gestation was examined. Fetal body growth was unchanged but brain cell DNA synthesis per gram of tissue decreased. Maternal serum levels of growth hormone and brain trophin were elevated following treatment conclusion. It was suggested that this was a rebound phenomenon and that short term blockade of pituitary growth hormone release during somatostatin treatment had impaired fetal brain cell DNA synthesis.
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PMID:The influence of maternal somatostatin administration on fetal brain cell proliferation and its relationship to serum gorwth hormone and brain trophin activity. 43 77

The effects of an 8-hour infusion of somatostatin, saline, gastrin or a mixture of gastrin + somatostatin on DNA synthesis and mitotic activity of gastrointestinal progenitor cells were explored in conscious rats, using in vivo labeling with 3H-thymidine and radioautography. Infusion of somatostatin (day or night) was shown to transiently reduce nuclear uptake of 3H-thymidine and cell division in both fundic and antral progenitor cells. Cell DNA synthesis in the gastrin + somatostatin-stimulated stomach was lower than in the gastrin-stimulated stomach. In the intestine, nocturnal infusion of somatostatin decrease DNA synthesis whereas diurnal infusion decreased cell division but no effect was observed on gastrin stimulation. Evidently, somatostatin may inhibit, perhaps indirectly, the cell proliferation in digestive mucosae and antagonize the trophic activity of gastrin but only in fundic and antral mucosae.
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PMID:Effect of somatostatin on normal and gastric-stimulated cell proliferation in the gastric and intestinal mucosae of the rat. 47 95

The ontogenesis of immunoreactive somatostatin in the embryonic and fetal rat pancreas has been measured by radioimmunoassay following acid extraction. Somatostatin (GIF) is detectable at 14 days gestation at a concentration of 1.6 X 10(-3) ng/pancreas. At term the content is 3.8 ng/pancreas, by 2 days neonatally, 8.3 ng/pancreas, and in the adult rat, 71 ng/pancreas through the concentration (expressed per microgram DNA) is constant from 14-19 days of gestation and reaches a level characteristic of the fully differentiated pancreas by birth. The detection of GIF in cultured pancreatic explants in the absence of innervation indicates that synthesis can occur independent of neural influence.
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PMID:The developmental pattern of somatostatin in the embryonic and fetal rat pancreas. 89 66

The aim of the present study was to examine the effects of melatonin (Mel) and of pinealectomy (PX) [in a long-term experiment in vivo - 10 weeks], as well as of Mel and N-acetylserotonin (NAc-5HT) [in experiments ex vivo in vitro and in vitro], on the rat thyroid growth processes. Additionally, the incubations in vitro of rat thyroid lobes with 3H-thymidine, in the presence of TSH, vasoactive intestinal polypeptide (VIP), VIP-antagonist ([4Cl-D-Ph6, Leu17]VIP), somatostatin (SS), all the substances used separately or jointly in combinations, were performed. It was shown that: (a) Mel--administered in late afternoon injections--decreased, while PX increased examined indices of thyroid growth in vivo, (b) Mel--administered in s.c. implanted pellets--reversed the inhibitory effect of Mel injections, (c) in experiments ex vivo in vitro and in vitro, the inhibitory effect of Mel revealed only for the lowest applied dose/concentration of the hormone, (d) NAc-5HT showed no effect, (e) VIP decreased 3H-thymidine incorporation into DNA of thyroid lobes in vitro and enhanced the inhibitory effect of SS on the process in question, (f) VIP-antagonist failed to reverse the inhibitory action of VIP on the thyroid growth.
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PMID:Effects of pineal-derived indolic compounds and of certain neuropeptides on the growth processes in the thyroid gland. 128 26

The presence of IGF-I and IGF-I receptors in human midgut carcinoid tumours has been investigated. Using immunocytochemistry, IGF-I-positive tumour cells were demonstrated in 11/11 tumour cases studied. Labelling of consecutive sections with antibodies against IGF-I and proliferating cell nuclear antigen (PCNA)/cyclin demonstrated a co-distribution of the 2 antigens in carcinoid tumours. Extracts of tumour tissues were subjected to radioimmunoassay and shown to contain significant amounts of IGF-I. Reverse-phase HPLC of tumour extracts demonstrated a major IGF-I-immunoreactive component eluting in the position of rhIGF-I, but also 2 other more hydrophobic forms. Conditioned serum-free media from primary cultures of carcinoid tumors contained detectable amounts of IGF-I, indicating a spontaneous release of IGF-I from tumour cells into the culture medium. Levels of IGF-I in media were reduced (19%) after incubation of cultures with a somatostatin analogue for 4 days. IGF-I receptors were observed on tumour cells in 4/10 tumours by immunocytochemistry. Tumour cells with immunoreactive IGF-I receptors could be stimulated to enhanced growth, measured as an increase in DNA contents, by exogenous administration of IGF-I every 3-4 days for 2 weeks. The results show that cultured human midgut carcinoid tumours secrete IGF-I and that some of the tumours also have IGF-I receptors. We therefore suggest that IGF-I may act as an autocrine or paracrine regulator of carcinoid tumour-cell growth.
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PMID:Presence of IGF-I in human midgut carcinoid tumours--an autocrine regulator of carcinoid tumour growth? 131 81

The thyroid follicular cell requires elevated levels of cAMP for normal growth and optimal expression of the differentiated phenotype. The recent discovery of cAMP-regulated enhancer binding (CREB) proteins prompted us to analyze the possible role of these transcription factors in controlling thyroid cell growth and differentiated phenotype using the FRTL5 thyroid cell line as a model system. FRTL5 cells were stably transfected with an expression vector containing either the gene for wild type CREB (WTCREB) or a dominant negative mutant form of CREB, termed KCREB, which dimerizes with and inactivates endogenous CREB. Transfected clones were found to express the transfected KCREB and WTCREB mRNAs at higher levels than the endogenous CREB mRNA. Transient expression of a somatostatin-chloramphenicol acetyltransferase fusion gene in these clones demonstrated a 60% reduction of cAMP-regulated enhancer-dependent transcriptional activity in the KCREB transfected clones and wild type levels of activity in the WTCREB transfected clones. Parameters of growth (DNA synthesis and growth rate) and differentiation (iodide uptake and thyroglobulin mRNA levels) were then analyzed in the transfected clones. Transfection of WTCREB had no effect on any of the parameters examined in comparison to untransfected cells, presumably because CREB is already constitutively expressed at maximal levels in normal FRTL5 cells. However, cells expressing KCREB showed an 18-40% reduction in TSH-stimulated thymidine incorporation, a 31% increase in the length of the cell cycle, and a 4-fold reduction in TSH-stimulated iodide uptake in comparison with wild type cells or cells tranfected with wild type CREB.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:3',5'-cyclic adenosine monophosphate-regulated enhancer binding (CREB) activity is required for normal growth and differentiated phenotype in the FRTL5 thyroid follicular cell line. 133 55


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