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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regulation of cholesterol ester synthesis was studied in cultured C-6 glial and neuroblastoma cells. Particular emphasis was placed on the relation of this regulation to control of cholesterol synthesis. The effectors studied were low density lipoprotein (LDL) and desmosterol. Distinct differences in regulation were observed between the glial and neuronal cells. In the neuronal cells cholesterol ester synthesis (from [14C]oleate) was not affected by even high concentrations of LDL or desmosterol. In contrast, cholesterol ester synthesis was stimulated as much as 12-fold in the glial cells after just 5 h exposure to LDL or desmosterol. Cholesterol synthesis (from [14C]acetate) was inhibited in a simultaneous and quantitatively similar manner. Suitable experiments indicated that alterations in pool sizes of intermediates did not contribute to the genesis of the observed responses and suggested that LDL and desmosterol produced their effects by stimulating esterification of primarily endogenous cholesterol. The data may have major implications concerning the controlling metabolic events prior to and at the onset of myelination.
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PMID:Regulation of cholesterol ester synthesis in cultured glial and neuronal cells. Relation to control of cholesterol synthesis. 20 52

When added to mouse neuroblastoma cultures, the potent tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) inhibits spontaneous neurite formation as well as that induced in response to serum deprivation, prostaglandin E1, 5-bromo-2'-deoxyuridine, and papaverine. Other tumor-promoting macrocyclic plant diterpenes also inhibit neurite formation, whereas nonpromoting diterpenes do not. Inhibition by TPA was reversible and was unrelated to toxicity.
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PMID:Tumor promoters inhibit morphological differentiation in cultured mouse neuroblastoma cells. 64 18

Regulation of cholesterol synthesis and, particularly, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase was studied in C-6 glial and neuroblastoma cells. Comparison of rates of incorporation of radioactivity from [14C]-acetate or [3H]mevalonate into digitonin-precipitable sterols indicated that HMG-CoA reductase is the major rate-limiting enzyme in cholesterol biosynthesis in both cell types. HMG-CoA reductase exhibited marked changes in enzymatic activity according to the lipoprotein content of the medium. However, significant differences were observed between the two cell types in the quantitative and temporal aspects of this regulation. Thus, in C-6 glial cells, when total serum lipoprotein was removed from the medium, reductase activity increased by 7-8-fold between 2 and 6 h later. After 24 h reductase activity in cells grown in lipoprotein-poor serum was 20-fold higher than in cells grown in regular serum. In neuroblastoma cells, under similar conditions, reductase activity did not increase at all until cells were in lipoprotein-poor serum for more then 6 h, and after 24 h, enzyme activity in cells grown in lipoprotein-poor serum was only approx. 3-fold higher than that in cells grown in regular serum. Addition of total serum lipoprotein caused a rapid decline in enzymatic activity in both cell types, with a t1/2 of 2-2.5 h; however, the onset of the decline was immediate in the glial cells but delayed 1-1.5 h in the neuronal cells. The critical regulatory component in the total lipoprotein fraction was shown to be contained in the low density lipoproteins for the reductase of both cell types. Regulation of reductase by free sterols was shown in both the glial and neuronal cells. However, effects were more marked and evolved more rapidly in the glial cells. The data thus provide important insight into the regulation of cholesterol synthesis in two cell types which are considered to be good models of neurons and glia of developing brain. The occurrence of more marked and more rapid regulation in the glial than in the neuronal cells is compatible with the important role glia play in brain lipid synthesis. The demonstration of dramatic regulation of HMG-CoA reductase by desmosterol, a sterol found in high concentration in brain early in development, may indicate a heretofore unrecognized role for this sterol in the regulation of cholesterol biosynthesis during maturation. 7-Ketocholesterol was shown to induce in C-6 glial cells a rate of decline of HMG-CoA reductase activity compatible with a t 1/2 of just 20 min. This extremely rapid rate of decline suggests that the effect involves an alteration in catalytic efficiency of the enzyme. The mechanism of this effect remains to be determined.
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PMID:Cholesterol biosynthesis and 3-hydroxy-3-methyl-glutaryl coenzyme A reductase in cultured glial and neuronal cells. Regulation by lipoprotein and by certain free sterols. 85 84

An analytical method is presented for determining cadmium, copper, and lead by differential pulse anodic stripping voltammetry and zinc by cathodic scan differential pulse voltammetry. Food samples are dry ashed using a sulfuric acid ashing aid, dissolved in dilute nitric acid, buffered at pH approximately 4.3 with an acetate buffer, and quantitatively analyzed using the technique of standard additions at a hanging mercury drop electrode. The quantitation limits (5 times the estimated detection limits) are approximately 5 ng/g for Cd, Cu, and Pb, and 50 ng/g for Zn. Accuracy of the method is established by (a) analysis of NBS Standard Reference Material No. 1577 Bovine Liver, (b) comparison of results obtained by the method described with those obtained by independent analytical methods, and (c) quantitative recovery of analyte metals from fortified, noncanned food samples. Results from an interlaboratory method trial indicate that the method is suitable for the analysis of a variety of food types.
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PMID:Dry ash-voltammetric determination of cadmium, cooper, lead, and zinc in foods. 89 6

The production and secretion of multiple peptide hormones and tyrosine hydroxylase by the human neuroblastoma cell line NB-1 and the effects of dibutyryl cAMP (Bt2cAMP) and phorbol esters such as 12-O-tetradecanoyl-phorbol-13-acetate (TPA) on them were investigated. The presence of messenger RNAs (mRNAs) of vasoactive intestinal peptide (VIP)/peptide histidine methionine (PHM), preprotachykinin, and tyrosine hydroxylase was detectable in the cytoplasm of cultured NB-1 cells by in situ hybridization. Treatment with Bt2cAMP and TPA markedly increased the number of cells immunoreactive to VIP, PHM, neuropeptide Y, Met-enkephalin, substance P and tyrosine hydroxylase and also the contents of VIP and Met-enkephalin in the culture medium. Bt2cAMP and TPA induced morphological changes characteristic of endocrine differentiation, such as an increase in neuroendocrine granules and the development of rough endoplasmic reticulum and Golgi apparatus. The results indicated that treatment with Bt2cAMP and TPA induces the expression of multiple genes of peptide hormone and tyrosine hydroxylase and increases hormone production and secretion through morphological changes into endocrine cells.
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PMID:Detection of multiple hormones and their mRNAs in human neuroblastoma cell line NB-1 using in situ hybridization, immunocytochemistry and radioimmunoassay. 127 91

The neuroblastoma line SK-N-SH consists of distinct and interconverting cell types, which include a neuroblast phenotype (SH-SY5Y), an epithelial phenotype (SH-EP), and an intermediate cell type (SH-IN). In SH-SY5Y cells, only muscarinic receptor activation produced stimulation of phosphoinositide turnover, whereas in SH-EP cells, where muscarinic receptors are not present, the peptides bradykinin, endothelin, and angiotensin II stimulated phosphoinositide hydrolysis with EC50 values of 16, 6, and 0.7 nM, respectively, and a rank order of maximal effects of bradykinin greater than endothelin greater than angiotensin II. Fetal calf serum at concentrations between 1 and 10% was also a potent stimulator of phosphoinositide hydrolysis in SH-EP cells but not in SH-SY5Y cells. In the intermediate cell clone, SH-IN, phosphoinositide hydrolysis was stimulated not only by muscarinic receptors, but also by endothelin, bradykinin, and serum, an indication that this cell type harbors all the kinds of receptors that are differentially expressed in the other two cell types. The effects of the three peptides--bradykinin, endothelin, and angiotensin II--on phosphoinositide hydrolysis in SH-EP cells were additive, a result suggesting that the three kinds of receptors may activate distinct transducer proteins and/or phospholipase C subtypes. Pretreatment of intact SH-EP cells with pertussis toxin under conditions sufficient to ADP-ribosylate 90-95% of the endogenous guanine nucleotide regulatory protein substrates did not impair the ability of any of the receptors to stimulate phosphoinositide hydrolysis in any of the cell types. In contrast, short-term exposure to the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (1 microM) abolished the stimulation of phosphoinositide hydrolysis mediated by peptide receptors in SH-EP cells and partially inhibited that by muscarinic receptors in SH-SY5Y cells. Prolonged incubation of SH-EP cells with phorbol ester resulted in a recovery of receptor responsiveness, the extent and rate of which were different for each receptor type. In contrast, there was no recovery of responsiveness for muscarinic receptors in SH-SY5Y cells. The pattern of phorbol ester-mediated effects depended on the cell rather than on the receptor type. In fact, muscarinic receptor responsiveness in SH-IN, the intermediate cell type, was desensitized by and recovered from treatment with phorbol esters in a manner more similar to peptide receptors in SH-EP than to muscarinic receptors in SH-SY5Y. These data suggest that the transduction mechanisms by which distinct receptor types are coupled to phosphoinositide hydrolysis in the three cell phenotypes differ in sensitivity to feedback regulation by protein kinase C.
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PMID:The epithelial phenotype of human neuroblastoma cells express bradykinin, endothelin, and angiotensin II receptors that stimulate phosphoinositide hydrolysis. 130 39

Neuronal differentiation was induced in cultures of the human neuroblastoma cell line subclone SH-SY5Y by 14-day treatment with dibutyryl cAMP (dBcAMP), retinoic acid, and phorbol 12-myristate 13-acetate (PMA). An approximate 4-fold increase in vasoactive intestinal peptide (VIP) mRNA concentration was observed after differentiation with retinoic acid, whereas no change in VIP mRNA concentration was observed after differentiation with dBcAMP or PMA. A short-term treatment of cells with PMA did however result in a 5-fold transient increase in VIP mRNA; prior differentiation with retinoic acid or dBcAMP diminished this effect. Observed increases in VIP mRNA were in all cases accompanied by increases in VIP immunoreactivity. Remarkably, however, long-term treatment of cells with dBcAMP, which caused no change in mRNA levels, resulted in a six-fold increase in VIP immunoreactivity. Acute (36-h) treatment with carbachol also caused an increase in VIP immunoreactivity (about 2-fold, and blocked by atropine) without an increase in VIP mRNA level. Thus, a quantitative change in gene transcription or mRNA stability appears not to be a prerequisite for increased VIP expression, indicating that regulation can occur at translational or post-translational steps.
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PMID:Distinct regulation of vasoactive intestinal peptide (VIP) expression at mRNA and peptide levels in human neuroblastoma cells. 131 16

Inositol 1,4,5-trisphosphate (InsP3) receptor immunoreactivity in SH-SY5Y human neuroblastoma cells was monitored with a monoclonal antibody raised against the mouse cerebellar InsP3 receptor. Recognition of a protein corresponding to the InsP3 receptor (molecular mass, approximately 275 kDa) was inhibited markedly following exposure of cells to 0.1 mM carbachol. This effect was half-maximal and maximal at approximately 2 and approximately 6 h, respectively; was blocked by atropine; but was not mimicked by thapsigargin, K+, or phorbol 12-myristate 13-acetate. However, the decrease in immunoreactivity following exposure of cells to carbachol for 5 h was blocked if the extracellular Ca2+ concentration was reduced from 1.3 mM to 200 nM. This manipulation also reduced markedly carbachol-induced increases in InsP3 concentration at 5 h. These data indicate that chronic muscarinic stimulation of phosphoinositide hydrolysis reduces InsP3 receptor concentration in SH-SY5Y cells, perhaps via a mechanism that involves prolonged elevation of InsP3 levels.
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PMID:Inositol 1,4,5-trisphosphate receptor immunoreactivity in SH-SY5Y human neuroblastoma cells is reduced by chronic muscarinic receptor activation. 131 71

To understand the cellular mechanisms that lead to the generation of synaptic plasticity of neuronal cells, it is important to understand the intracellular responses of neuronal cells stimulated via synaptic transmission. The stimulation of mouse cerebellar granule cells via NMDA (N-methyl-D-aspartate) receptors caused an increase in deoxyribonucleic acid (DNA)-binding activities to TRE (12-O-tetradecanoylphorbol-13-acetate-responsive element) and CRE (adenosine 3',5'-cyclic monophosphate-responsive element) motifs, depending upon the presence of extracellular Ca2+. The increases in TRE- and CRE-binding activities were also detected with the stimulation of non-NMDA receptors by kainate. The increases in TRE- and CRE-binding activities were both mediated by the same DNA-binding complexes whose binding affinity to CRE was about three-fold higher than that to TRE. On the other hand, the stimulation of neuroblastoma x glioma hybrid NG108-15 via muscarinic acetylcholine receptors, alpha 2-adrenergic receptors and bradykinin receptors caused a rapid induction of zif/268. An additive effect on the induction of zif/268 was observed when the different stimuli were simultaneously added. Thus, it is extremely likely that signals transduced via synaptic transmission are transferred to the level of gene expression and evoke some events which might contribute to the generation of synaptic plasticity in neuronal cells. In addition, we have found that the direct injection of plasmid DNAs into mouse skeletal muscle with fructose, glucose or NaCl solution led to a long-term expression of the introduced gene in muscle cells.
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PMID:[Genetical responses of neuronal cells to synaptic transmission]. 132 98

The signal transduction systems of the neuropeptide Y (NPY) Y1 receptor were studied in SK-N-MC human neuroblastoma cells. NPY induced an increase in intracellular calcium ion concentration ([Ca2+]i) and inhibition of forskolin-stimulated cyclic AMP accumulation, which were mediated through Y1 receptors. One-min preincubation of cells with phorbol 12-myristate 13-acetate (PMA) inhibited both signal transductions dose-dependently, but its effect on [Ca2+]i was about 100-fold more potent than that on cyclic AMP. PMA had no effect on [125I]BH-NPY binding in SK-N-MC cells and hardly inhibited the endothelin-1-induced increase in [Ca2+]i. Pertussis toxin also inhibited the NPY-induced [Ca2+]i increase 30-fold more effectively than the NPY-mediated inhibition of cyclic AMP accumulation. These results indicate that Y1 receptors in SK-N-MC cells couple to two signal transduction systems that have different sensitivities to phorbol ester and pertussis toxin treatments.
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PMID:Two different signal transductions of neuropeptide Y1 receptor in SK-N-MC cells. 132 39


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