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)

Regulation of adenohypophyseal hormone secretions has been shown to involve cyclic AMP production, modulation of phosphatidyl inositol diphosphate breakdown and Ca2+ mobilization. Various neurohormone receptors are positively or negatively coupled to adenylate cyclase activity in anterior pituitary cells. The effects of these neurohormones on adenylate cyclase activity are consistent with the effect on hormone secretions, suggesting that modulation of the enzyme activity is actually involved in the regulation of adenohypophyseal secretions. Thus DA inhibits, whereas VIP stimulates adenylate cyclase activity of the same cell type, which, according to the effect of these neurohormones on prolactin secretion, appear to be lactotrophs. On the other hand, SRIF inhibits, whereas GRF stimulates the adenylate cyclase activity of another cell type, namely somatotrophs, whereas CRF appears to act on a third cell type, corticotrophs. Peripheral hormones have been shown to modulate the sensitivity of anterior pituitary cells to these neurohormones. Estradiol long-term treatment has an anti-dopaminergic effect on prolactin secretion. The steroid also suppresses the dopamine inhibition of adenylate cyclase. This effect appears selective to the DA inhibition, since AII inhibition of the enzyme is only partially reduced, whereas the somatostatin inhibition is markedly increased. Peripheral hormones seem to affect the sensitivity of adenohypophyseal cells not only by modulating the number of receptors for a given neurohormone but also by interfering with the coupling mechanisms of these receptors. AII and DA inhibit the adenylate cyclase activity of lactotroph cells. The prolactin stimulation induced by angiotensin is not consistent with the effect of the peptide on adenylate cyclase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple coupling of neurohormone receptors with cyclic AMP and inositol phosphate production in anterior pituitary cells. 282 May 13

Examination of gastrin-immunoreactive G-cells, somatostatin-immunoreactive D-cells, enterochromaffin cells and 5-hydroxytryptamine-immunoreactive (5-HT-immunoreactive) cells of the completely mapped histologic antrum (70 to 100 tissue blocks) was done in 20 normal stomachs of persons between 17 and 94 years of age (from forensic autopsy). Results were compared with those of nine patients between 48 and 76 years of age with total gastrectomy for carcinoma of the proximal part of the stomach. Cell counts and morphometric examinations were performed. Results were summarized for the proximal (I), middle (II) and distal (III) one-third of the antrum and for the major (A) and minor (B) curvature side. In normal stomachs, the G-cell count was 2.52 percent of the total gland cell count in AI; 4.25 percent in AII and 4.77 percent in AIII. In BI, the numbers were 2.5 percent, in BII, 3.73 percent and 4.06 percent in BIII. The D-cell count was 0.47 percent in AI, 0.62 percent in AII and 0.58 percent in AIII. The numbers were 0.44 percent in BI, 0.51 percent in BII and 0.51 percent in BIII. In the antrum of the stomach with carcinoma, the G-cells revealed a non-significant 20 to 70 percent lower cell count, while the D-cell count was reduced insignificantly by as much as 35 percent in all areas. The 5-HT-immunoreactive cell count in normal stomachs is 0.25 percent in AI of the total gland cells, 0.32 percent in AII and 0.39 percent in AIII. In B, it shows numerically no difference to that of A. Contrary to the cell count in normal stomachs, the carcinoma antrum revealed a 200 to 400 percent increase in 5-HT-immunoreactive cell count, highly significant in every area of the antrum. Because 5-HT is known as a growth stimulant, especially for tumors, an increase in 5-HT-immunoreactive cells may be a factor that contributes to the initial histologic changes observed during the early phase of gastric tumor.
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PMID:Histologic, immunohistochemical and morphometric study of the mucosa of the total gastric antrum in patients with carcinoma of the stomach. 809 84

Caldendrin is a novel calcium-binding protein confined to the somatodendritic compartment of neurons. Here we have studied the expression pattern of caldendrin in the rat retina. First we assessed the distribution of caldendrin transcripts in the adult and developing retina by in situ hybridization. In the adult retina, transcripts are expressed mainly in the inner half of the inner nuclear layer (INL) and to a lesser extent in the ganglion cell layer (GCL). During development labeling of the inner part of the cytoblast layer, where amacrine cells reside, is already present at postnatal day 1 (P1). The intensity of hybridization signal in this sublamina of the developing INL increases up to P8, whereas significant labeling in the GCL was first found at P14, coinciding with eye opening. Immunodetection with a polyclonal antibody revealed intensive staining of cells in the inner retina, which are presumably mainly amacrine and significantly fewer bipolar and ganglion cells. All parvalbumin-containing All amacrines were immunopositive for caldendrin. Colocalization with calbindin was found in cone bipolar cells, the majority of AII amacrines, and calbindin-positive cells in the GCL. In the GCL, caldendrin was also colocalized with calretinin-immunopositive cells. Most caldendrin-positive amacrine cells in the adult rat retina were glycinergic and only a few were GABAergic. In retinal flat mounts, it was confirmed that less than 10% of retrogradely labeled retinal ganglion cells (RGC) are caldendrin-positive. Caldendrin immunoreactivity does not colocalize with tyrosine hydroxylase, VIP, substance P and somatostatin immunoreactivity. In summary, caldendrin expression is regulated differentially in retinal cell types during development and is restricted to a subpopulation of amacrine, bipolar, and ganglion cells, suggesting specific functions in the developing and mature retina.
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PMID:The cytoskeleton-associated neuronal calcium-binding protein caldendrin is expressed in a subset of amacrine, bipolar and ganglion cells of the rat retina. 1055 36

To investigate the molecular mechanism(s) of action of catecholamines on the expression of the angiotensinogen (ANG) gene in kidney proximal tubular cells, we used opossum kidney (OK) cells with a fusion gene containing the 5'-flanking regulatory sequence of the rat ANG gene fused with a human growth hormone (hGH) gene as a reporter, pOGH (rANG N-1498/+18), permanently integrated into their genomes. The level of expression of the ANG-GH fusion gene was quantified by the amount of immunoreactive-hGH (IR-hGH) secreted into the medium. The addition of norepinephrine (NE), isoproterenol (a beta1/beta2-adrenergic receptor (AR) agonist) and iodoclonidine (an alpha2-AR agonist) stimulated the expression of the ANG-GH fusion gene in a dose-dependent manner, whereas the addition of epinephrine and phenylephrine (alpha1-AR agonist) had no effect. The stimulatory effect of NE was blocked by the presence of propranolol (beta-AR blocker), atenolol (beta1-AR blocker), yohimbine (alpha2-AR blocker), Rp-cAMP (an inhibitor of cAMP-dependent protein kinase AI & AII) and staurosporine (an inhibitor of protein kinase C), but was not blocked by ICI 118, 551 (beta2-AR blocker) and prazosin (alpha1-AR blocker). The addition of a combination of isoproterenol and iodoclonidine or a combination of 8-Bromo-cAMP (8-Br-cAMP) and phorbol 12-myristate (PMA) synergistically stimulated the expression of the ANG-GH fusion gene as compared to the addition of isoproterenol, iodoclonidine, 8-Br-cAMP or PMA alone. Furthermore, the addition of NE, 8-Br-cAMP or PMA stimulated the expression of pOGH (rANG N-806/-779/-53/+18), a fusion gene containing the putative cAMP responsive element (CRE, ANG N-806/-779) upstream of the ANG promoter (ANG N-53/+18) in OK cells, but had no effect on the expression of fusion genes containing the mutant of the CRE. Gel mobility shift assays revealed that the ANG-CRE binds with the DNA-binding domain (bZIP254-327) of the cAMP-responsive binding protein (CREB). The binding of the labeled ANG-CRE to CREB (bZIP254-327) was displaced by unlabeled ANG-CRE and the CRE of the somatostatin gene but not by the mutants of the ANG-CRE. Finally, NE stimulated the phosphorylation of CREB in OK cells. These studies demonstrate that the molecular mechanism(s) of NE action on the expression of the ANG gene in OK cells may be mediated via both the PKA and PKC signalling pathways and via the phosphorylation of CREB. The phosphorylated CREB then interacts with the CRE in the 5'-flanking region of the ANG gene and subsequently stimulates the gene expression.
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PMID:Catecholamines and angiotensinogen gene expression in kidney proximal tubular cells. 1110 38

Transient retinal ischemia induces loss of retinal ganglion cells, supporting the hypothesis that ischemic conditions contribute to the induction and progression of glaucoma. However, after 60 min of ischemia, also amacrine cells are lost from the inner nuclear layer. The main goal was to determine the relative vulnerability of various amacrine subpopulations by measuring the levels of transcripts that are known to be specifically expressed by different amacrine subpopulations. A 60-min ischemic period was administered to the rat eye by raising the intraocular pressure, followed by a reperfusion period lasting between 2 h and 4 weeks. Total RNA was isolated from the whole retina and expression levels were assessed by real-time quantitative polymerase chain reaction (qPCR). Retinal ischemia/reperfusion has differential effects on the levels of the various transcripts. Three main patterns of changes were identified. (i) A gradual decrease of transcript level without recovery was observed for parvalbumin; this transcript is expressed by the glycinergic AII cells. (ii) A gradual reduction to different levels at 72 h of reperfusion followed by a partial or complete recovery (glycine transporter 1, glutamate decarboxylase, calretinin, and several other transcripts). The glycinergic amacrine cell markers recovered to 65-75% of the control level, while the main GABAergic markers had completely recovered at 4 weeks. (iii) No significant changes of transcript levels were found for markers of several smaller GABAergic subpopulations [including substance P (Tac1), somatostatin, and others]. Expression levels of photoreceptor-, horizontal cell-, and bipolar cell-specific transcripts were not altered. These patterns were confirmed by a cluster analysis of the data. Based on gene expression levels, it may be concluded that amacrine cells are vulnerable to ischemic insults and that the glycinergic amacrine cells are relatively more sensitive to ischemia than the GABAergic population. In particular, the extensive loss of the parvalbumin-containing AII amacrine cells, which serve in the rod pathway, may have functional implications for vision under scotopic conditions. In the accompanying paper [F. Dijk and W. Kamphuis, An immunocytochemical study on specific amacrine subpopulations in the rat retina after ischemia, Brain Res. (2004).], the results are evaluated at the protein level by immunostaining for a selection of the amacrine cell markers.
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PMID:Differential effects of ischemia/reperfusion on amacrine cell subtype-specific transcript levels in the rat retina. 1548 81

Somatostatin (SRIF), as a neuroactive peptide in the CNS, exerts its actions via five subtypes of specific receptors (ssts). In this work, the localization of sst(5) was studied immunocytochemically in rat retinal amacrine cells (ACs). Labeling for sst(5) was diffusely distributed throughout the full thickness of the inner plexiform layer (IPL) and formed two distinct fluorescence bands in the distal part of the IPL. Double labeling experiments showed that sst(5) was expressed in GABAergic ACs. It was further shown that labeling for sst(5) was observed in both dopaminergic and cholinergic ACs, stained by tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT), respectively. The immunostaining appeared mainly on the cell membranes and somatodendritic compartments of these ACs. For the cholinergic ACs, weak sst(5)-immunoreactivity was also observed in the processes terminating in the IPL. In contrast, no sst(5)-immunoreactivity was found in glycinergic AII ACs, stained by parvalbumin (PV). Furthermore, labeling for SRIF was co-localized with sst(5) in both dopaminergic and cholinergic ACs. These results suggest that sst(5) may serve as an autoreceptor or conventional receptor in retinal ACs.
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PMID:Expression of somatostatin receptor subtype 5 in rat retinal amacrine cells. 1715 33