Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A nasal neuroblastoma (esthesioneuroblastoma) extending into the brain in a heifer produced mouth breathing and proptosis. The mass filled much of the left nasal cavity, palatine sinus and maxillary sinus, with turbinate atrophy and deviation of the septum. Caudally the neoplasm extended into the nasopharynx and olfactory bulb. It was a cellular neoplasm composed of small, undifferentiated piriform cells showing infrequent pseudorosettes and immature axonal processes. Mitosis was common is some areas.
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PMID:Olfactory neuroblastoma in a heifer. 725 93

Bovine brain gangliosides were applied to primary and established neuronal cultures to examine the role of gangliosides in neuronal development. Media containing gangliosides enhanced the degree of axonal elongation exhibited by sensory ganglia neurons and increased the length and number of Neuro-2a neuroblastoma cell processes. Ganglioside-supplemented media caused a twofold increase in ornithine decarboxylase activity in both culture systems. These experiments suggest that gangliosides function as acceptor molecules for growth-promoting substances in embryonic and tumor-derived neurons.
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PMID:Ganglioside stimulation of axonal sprouting in vitro. 729 99

To investigate further the selectivity of retrograde axonal transport of horseradish peroxidase (HRP) isoenzymes previously observed in the rat central visual pathways, cultured mouse neuroblastoma cells (clone N18) were examined for selectivity of endocytosis of peroxidases and cationized ferritin in vitro. Differentiating N18 cells were incubated with proteins in various timing and pulse-chase experiments, and examined for the ultrastructural localization of endocytosed protein using cytochemical techniques. Semi-quantitative morphometry was performed on some of the samples. Major findings were as follows. (1) The protein was internalized into vesicles (coated and uncoated), short tubules and occasional small cup-shaped bodies within the first few minutes, and transferred via tubules and uncoated vesicles to secondary lysosome-like organelles (vacuoles, multivesicular bodies and dense bodies) from 5 to 15 min, with dense bodies representing the final site of protein accumulation. All the proteins tested were endocytosed through the same pathways in the soma and neurite of the cell. (2) There was no indication of a net orthograde or retrograde neuritic transport proteins. (3) There were induced increases in both vesicle and tubule formation as a result of protein endocytosis, with HRP isoenzyme C showing the greatest effect. (4) The apparent rate of internalization of HRP isoenzyme C into vesicles during the initial 5 min was significantly greater than for other peroxidases amd cationized ferritim. (5) Relatively more tubules than vesicles were involved in the uptake of protein as endocytosis was prolonged from 5 min to 8 h, with HRP isoenzyme C showing the largest effect. (6) There were indications of preferential compartmentation of endocytosed protein into certain organelles.
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PMID:Endocytosis and compartmentation of peroxidases and cationized ferritin in neuroblastoma cells. 744 Dec 98

The endocytotic uptake and intracellular decay of horseradish peroxidase isoenzymes C and A by cultured mouse neuroblastoma cells were analyzed quantitatively by a direct spectrophotometric assay. At concentrations below 1 mg/ml, the rate of uptake of the isoenzyme C was more than three times as much as the isoenzyme A. This differential uptake suggests that previous claims of horseradish peroxidase being endocytosed only in the nonselective fluid phase are oversimplified. The implication of this selectivity in the biological significance of retrograde axonal transport of proteins by neuronal systems is discussed.
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PMID:Differential uptake of horseradish peroxidase isoenzymes by cultured neuroblastoma cells. 746 60

The axonal microtubule-associated protein, tau, is thought to play an important role in axonal growth and in the establishment of neuronal polarity. In adult human brain there are six alternatively spliced tau isoforms, which have different microtubule binding affinities in vitro. The tubulin-tau interaction is further modified by phosphorylation of tau and, compared to adult brain tau, both foetal brain tau and paired helical filament (PHF) tau, characteristic of Alzheimer's disease, are hyperphosphorylated. In vivo both the expression of tau isoforms and their phosphorylation states are developmentally regulated. In order to establish the correlation between the expression of tau isoforms and their pattern of phosphorylation, we have characterised these two features in several in vitro models of neuronal differentiation, including the human neuroblastoma cell lines, SK-N-SH, SH-SY5Y and IMR32 cells, rat PC12 cells and primary rat cortical neurones. Sensitive RT-PCR analysis revealed a different complement of tau isoforms in the different cell lines and neuritogenesis was associated mainly with an increase in the overall tau protein level with no apparent phosphorylation changes. A switch in tau isoform expression occurred only at the terminal stages of neuronal development, when it may be important in reinforcing the previously established axonal cytoarchitecture.
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PMID:Tau isoform expression and phosphorylation state during differentiation of cultured neuronal cells. 749 9

Cisplatin causes a dose limiting peripheral neuropathy, however, the biological mechanism by which this occurs is unknown. Murine N1E.115 neuroblastoma cells and neural crest derived pigment cells have similar transport mechanisms to human neural cells and were used to study the effect of cisplatin on cellular transport. Cisplatin reduced both the number and velocity of organelles moving in the anterograde and retrograde direction, compared to control cells. Cisplatin induced inhibition of transport was prevented by the simultaneous administration of ACTH4-9. This analog alone had no effect on N1E.115 organelle, or erythrophore granule, movement. In both N1E.115 and pigment cells cisplatin inhibited transport within 1 h of exposure to the drug. The degree of inhibition did not increase insignificantly if pigment cells were incubated in cisplatin for 48 h compared to acute exposure. Microtubules in both pigment cells and N1E.115 neurites retained their structural integrity suggesting that factors other than changes in gross microtubule morphology are responsible for cisplatin neurotoxicity. Cisplatin reduces N1E.115 neurite growth after 48 h incubation but this can be prevented by simultaneous use of ACTH4-9. This study demonstrates for the first time that cisplatin and ACTH4-9 affect fast axonal transport by specific mechanisms which appear related to their observed neurotoxic and neuroprotective roles, respectively.
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PMID:Effect of cisplatin and ACTH4-9 on neural transport in cisplatin induced neurotoxicity. 761 95

It has been suggested that G0 and Gi play a role in the collapse of axonal growth cones and the retraction of neurites. We have studied the G-protein content of neuroblastoma cells undergoing neurite outgrowth and subsequent retraction in response to neocarzinostatin (NCS). Stimulators of G0 and Gi have no effect upon neurite outgrowth or retraction and the cellular content of G0 and Gi does not change during the course of these morphological phenomena. Modulation of G-protein content, therefore, most likely does not play a role in this process.
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PMID:G-protein expression during enediyne-induced neurite outgrowth in neuroblastoma. 775 74

NSC-34 is a hybrid cell line produced by fusion of motor neuron enriched, embryonic mouse spinal cord cells with mouse neuroblastoma. Cultures contain two populations of cells: small, undifferentiated cells that have the capacity to undergo cell division and larger, multi-nucleate cells that express many properties of motor neurons. The utility of NSC-34 cells as a model for investigation of neurotoxicity was evaluated following exposure of cultures to a selection of chemicals known to be neurotoxic to motor neurons. NSC-34 responded to agents that affect voltage-gated ion channels, cytoskeletal organization and axonal transport. The sensitivity of action potential production to various ion channel blockers was similar to that in primary motor neurons in culture. 2,5-hexanedione induced focal aggregation of neurofilaments in perikarya and processes of NSC-34. Sodium pyridinethione induced swelling and retraction of processes. In contrast, NSC-34 was not a good model in which to investigate agents that affect synaptic transmission. No electrophysiological evidence of synaptic connections between NSC-34 cells was obtained. Exposure to 1 mM glutamate had no effect on cell morphology or action potential production. Difficulties in using this line to investigate chemical neurotoxicity were poor substrate adhesion, requirement for routine subculture and change in expression of the neuronal phenotype with repeated subculture.
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PMID:Evaluation of the spinal cord neuron X neuroblastoma hybrid cell line NSC-34 as a model for neurotoxicity testing. 790 62

To test the hypothesis that glial-derived factors exert differential effects on neurons in developing and aged brain, we treated NB2a/d1 neuroblastoma cells with conditioned medium (CM) obtained from C6 glioma cells. Undifferentiated NB2a/d1 cells rapidly (< 4 h) elaborated neurites in response to CM. Cells previously differentiated by 14 days treatment with 1 mM dbcAMP, which induces outgrowth of axonal neurites, exhibited no obvious effects when exposed to CM. By contrast, CM was toxic to cells that were treated with 1 mM dbcAMP for 7 days followed by 7 days in which dbcAMP had been reduced to 0.1 mM or withdrawn. These results highlight the potential of glial-derived factors to exert trophic and toxic effects depending upon neuronal differentiation state.
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PMID:Toxic and trophic effects of glial-derived factors on neuronal cultures. 801 52

This study shows that the fish optic nerve, which is able to regenerate after injury, contains myelin-associated growth inhibitors similar to the growth inhibitors present in mammalian central nervous system (CNS) myelin. The ability of nerves to regenerate was previously correlated with the ability of sections from these nerves to support neuronal attachment and axonal growth in vitro. Thus neuroblastoma cells or embryonic neurons became attached to and grew axons on sections of rat sciatic nerve or fish optic nerve, which are spontaneously regenerating systems, but not on sections of rat optic nerve, a nonregenerating system. Failure of the latter to support axonal growth has been attributed, at least in part, to growth inhibitors. Recently it was shown that adult neurons, which differ in their growth requirement from embryonic neurons, are unable to extend neurites on sections of normal sciatic nerve but are able to extend neurites on sections of sciatic nerve that was injured prior to its excision. We found a similar situation in the fish optic nerve, i.e., that the nerve is normally not permissive to growth of adult retinal axons but becomes growth permissive after injury. The nonpermissiveness of the normal fish optic nerve was found to correlate with the presence of myelin-associated growth-inhibitory molecules. This inhibitory activity of fish myelin was neutralized by IN-1 antibodies, known to neutralize rat myelin growth inhibitors. The results thus demonstrate that fish optic nerve myelin contains inhibitors apparently similar or even identical to those of rat, but possibly present in lower amounts than in the rat. Results are discussed with respect to the possibility that fish optic nerve, like the rat sciatic nerve and unlike the rat optic nerve, undergoes certain changes after injury that support regeneration of adult neurons. Such changes might include elimination or neutralization of growth inhibitors.
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PMID:Presence of growth inhibitors in fish optic nerve myelin: postinjury changes. 802 41


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