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)

Laminin and fibronectin, the major noncollagenous matrix glycoproteins, were studied in connection with normal brain cells and neuroectodermal cell lines. Laminin, a Mr 900,000 dalton matrix glycoprotein and an essential component of basement membranes, was found to be produced by cultured cells of several malignant cell lines of neuroectodermal origin. In cultured mouse C1300 neuroblastoma line cells laminin was localized, by immunoelectron microscopy, to the rough endoplasmic reticulum and, to sites of cell-to-cell and cell-to-substratum adhesion. Further experiments on the intracellular transport of this glycoprotein in C1300 cells confirmed that laminin is, at least partially, transported through the Golgi pathway. These results favor a role for laminin in attachment and cellular interactions of malignant neuronal cells. Laminin was also found in connection with neurons and glial cells from mammalian brain. In primary cultures from developing rat brain the vast majority of non-neuronal cells (80%) expressed immunoreactivity for the glial fibrillary acidic protein, a cytoskeletal protein specific for astrocytes. During the first week in culture all the glial fibrillary acidic protein-positive cells, with the exception of mature-looking star-shaped astrocytes, exhibited immunoreactivity for laminin. The intracellular laminin disappeared gradually after a few weeks in culture, but an extensive laminin matrix persisted and seemed to be localized on the upper surface of the non-neuronal cells. The neurofilament-positive neurons were negative for laminin. Pretreatment of the cultures with the ionophore monensin, caused accumulation of laminin-immunoreactivity within the Golgi region, which confirmed that laminin is, indeed, produced by cultured astrocytes and secreted through the Golgi complex. No fibronectin immunoreactivity was found in the majority of glial cells. However, under culture conditions where fibronectin was omitted from the culture medium there was, in the primary cultures, a minor population of glial fibrillary acidic protein-positive flat glial cells that exhibited intracytoplasmic immunofluorescence for fibronectin. In the presence of fibronectin in culture medium no fibronectin-positive glial cells could be detected. It thus appears that laminin, and to a minor extent fibronectin, are proteins that normal glial cells are capable of producing under specific conditions. Laminin and fibronectin were localized in adult rat brain in capillary and meningeal structures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Laminin and fibronectin in normal and malignant neuroectodermal cells. 638 23

The minor active component of bee venom was applied to mouse neuroblastoma cultures. The cytological changes observed are reported. After 8-10 h of incubation with 5 micrograms/ml of apamin in the culture medium, considerable retractions of the processes are apparent. Electron microscopically, the alterations seen are predominantly found in the subcellular organelles. The peculiar configuration of the endoplasmic reticulum (ER) is striking. Concentric whorls of cisternae seem to engulf the remaining ground substance. Following a 24-hour incubation with 5 micrograms/ml of apamin, the cell membrane disintegrates. A deeply infolded nucleus, vacuoles and remnants of cell organelles are present. The previously intact synapses are totally degenerated. Similar experiments using lower concentrations of apamin do not depict any apparent changes either light or electron microscopically.
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PMID:Changes induced by apamin from bee venom on differentiated mouse neuroblastoma cells in culture. 666 37

Laminin was localized in cultured mouse C1300 neuroblastoma cells by applying the peroxidase-antiperoxidase technique in preembedding electron microscopy. The results were compared to those obtained by indirect immunofluorescence and by the colloidal gold second antibody method on Epon-embedded ultrathin sections. Laminin was found in the cell membranes and within the rough endoplasmic reticulum as well as in intracytoplasmic vacuoles. Plasma membranes of the neuroblastoma cells showed a patchy localization of laminin that was apparently involved in cell-to-substrate attachment and in gap junction-like intercellular connections. Under normal conditions, the Golgi cisternae contained no laminin. Pretreatment of cells with micromolar concentrations of monensin, however, lead to an accumulation of laminin within the Golgi cisternae. These results support a role for laminin as an adhesion protein in cultured neuroblastoma cells and indicate that laminin is transported through the Golgi complex.
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PMID:Laminin in cultured mouse C1300 neuroblastoma cells: immunocytochemical localization by pre- and postembedding electron microscope procedures. 684 71

Sera from a patient with systemic lupus erythematosus (SLE), tested by indirect immunofluorescence on frozen tissue sections, gave granular cytoplasmic staining of hepatocytes, gastric chief cells, exocrine cells of the pancreas and submandibular glands, and cerebellar Purkinje cells. In acetone-fixed monolayers of rat embryonic fibroblasts, 3T3 cells, mouse neuroblastoma cells, and cells from a human melanoma and colon carcinoma cell line, the sera stained perinuclear cytoplasmic granules which radiated out towards the cell periphery. More mature and differentiated fibroblasts from rat of human foetal lung showed staining of reticular cytoplasmic structures corresponding to phase-dense rough endoplasmic reticulum (RER). Nucleoli were prominently stained in all cultured cells. Serum absorption with ribosomes inhibited all antibody activity but absorption with RNA or with RNase-treated ribosomes resulted only in partial inhibition. Monolayers of RNase-treated fibroblasts gave weaker staining reactions compared to control untreated cultures. These observations suggest that the autoantibody is directed against ribosomal RNA and ribosomal protein present in cytoplasmic polyribosomes, in RER and in nucleoli.
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PMID:Autoantibody to ribosomes and systemic lupus erythematosus. 700 92

Sodium bromide was applied in vitro to mouse neuroblastoma cells of different ages for short and long periods (2 h to 10 days). The changes observed light-and-electron microscopically were similar to those described earlier after GABA treatment. Coated vesicles proliferated and originated by pinching off from the Golgi complex and from the rough endoplasmic reticulum. Numerous coated vesicles were continuous with the plasma membrane, especially near zones in which electron-dense material aggregated at the inner aspect of the plasmalemma. Small invaginations, similar in ultrastructure to coated vesicles, were also formed. It is unclear whether the coated vesicles or the dense plasmalemma invaginations contribute to the "undercoating" by fusing with the adjacent electron-dense plasma membrane. There was a distinct increase in the number and area of specialized contacts (intermediate junctions and zonulae adhaerentes) between cells and their processes. A floccular or filamentous electron-dense substance varying in amount and appearance was occasionally seen between the contacting membranes. Varicosities of terminal swellings of cell processes contained vesicles of variable size, shape and density, and also profiles of the smooth endoplasmic reticulum. Under the influence of sodium bromide, similar to the effect of GABA, mitochondria appeared within the varicosities, and primitive contacts (intermediate junctions) were formed between the terminal swellings and potential postsynaptic elements, which were absent in controls. Additionally, dense-core vesicles proliferated and aggregated at the cell periphery. They were often arranged linearly below the plasma membranes of perikarya and processes, and surrounded by a highly electron-dense substance. The similarity of the present findings to those obtained after GABA treatment and their relation to synaptogenesis are discussed.
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PMID:Morphological changes induced by sodium bromide in murine neuroblastoma cells in vitro. 708 7

Growth cones of 'differentiating' neuroblastoma cells in monolayer culture were studied by time-lapse cinematography and electron microscopy. Morphological differentiation, and thus growth cone formation, was induced by the glucocorticoid dexamethasone. Growth cones lengthened gradually at an average rate of 30 microns/h, advancing in stages that involved alternating extensions and retractions of the filopodia and lamellar sheets. During neurite growth the cell body usually remained stationary. The ultrastructure of growth cones was typified by several filopodia, each containing a bundle of microfilaments, agranular endoplasmic reticulum, aggregates of large agranular vesicles lying adjacent to filopodia (previously termed vesicle-filled mounds), many dense-cored vesicles, 100-140 nm in diameter, microtubules, bizarre and distorted mitochondria, and scattered from ribosomes. Comparing the findings with previous ultrastructural accounts of growth cones of cultured ganglion cells, similarities outnumbered differences. The organization of the microfilament bundles and the abundance of free ribosomes were remarkable in the neuroblastoma cell as was the profusion of dense-cored vesicles which were most numerous in the proximal portion of the growth cone.
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PMID:Growth cones in differentiated neuroblastoma: a time-lapse cinematographic and electron microscopic study. 719 11

(Gamma aminobutyric acid) GABA was applied to cultures of mouse neuroblastoma cells of different ages at concentrations ranging from 10(-4) to 10(-6) M. The cultures were exposed to GABA either in short term experiments for 2 h to 2 days or for longer periods by adding the substance twice within 10 days at 5-day intervals. The following effects were observed: (1) There was a strong proliferation of coated vesicles, appearing to derive from the Golgi complex and the rough endoplasmic reticulum (RER), and also showing all intermediate stages of fusion and pinching off from the plasma membranes. (2) In numerous areas, electron-dense material aggregated at the inner aspect of the plasma membrane and around small invaginations of the plasmalemma. (3) The number and area of specialized contacts increased between cells and their processes. (4) Similar to cultures free of GABA, varicosities and terminal swellings of the cells and their processes were filled with small round vesicle, 40--60 nm in diameter, or with smooth, very large, empty-appearing vesicular inclusions, or with flat pleiomorphic vesicles. In addition, mitochondria and some formations of the smooth endoplasmic reticulum (SER) appeared, and primitive contacts (symmetrical densities) were formed. (5) Dense-cored vesicles were found peripherally and linearly arranged, surrounded by an electron-dense substance. (6) Electron-dense material of unknown origin was seen between cells or their processes near the peripherally arranged dense-cored vesicles. Exogenous GABA may play a specific role in the early stages of synaptogenesis, since it showed a positive effect on the neuroblastoma cells, which in the absence of GABA are only capable of forming primitive or immature presynaptic elements. The significance of the peripheral accumulation of dense-cored vesicles, accompanied by an amorphous, electron-dense substance occurring both intra- and extracellularly is discussed.
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PMID:Effect of GABA-administration on murine neuroblastoma cells in culture. I. Increased membrane dynamics and formation of specialized contacts. 726 Oct 42

Cultured murine neuroblastoma cells contain an extensive smooth endoplasmic reticulum (SER), also within their numerous processes and their terminals, consisting of a complex network of sacs and tubules. Both the perikaryal and the SER found within the processes and endings resemble one another morphologically. From the SER whether it is within the perikaryon or within the terminals of the neural processes, round coated vesicles with clear centers appear to form. These clusters of vesicles are 40...60nm in diameter and indistinguishable from the synaptic vesicles of normal neurons. In addition a few vesicles with clear centers with a diameter of 20...40 nm and length of 80...200 nm are encountered and appear to originate from the SER. The dense-cored vesicles do not seem to develop from the SER. There is no detectable association of the vesicles with any other cell organelle.
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PMID:Smooth endoplasmic reticulum and synaptic vesicles in cultured murine neuroblastoma cells. 730 12

Cell cultures of the continuous human neuroblastoma lines SK-N-SH, SK-N-BS(2), and SK-N-MC at exponential and stationary growth phase have been examined by electron microscopy. At the level of fine structure these cells did not show typical neuronal differentiation such as extensive granular endoplasmic reticulum or neurites with microtubules and neurofilaments. Instead they were characterized by abundant free ribosomes, moderate Golgi complexes, and usually scant granular endoplasmic reticulum, features similar to the fine structure of early normal embryonic autonomic neurons. However, in several respects appearance of differentiated features of the neuroblastoma cells did not follow the pattern observed for normal neurons, suggesting noncoordinate expression of neuronal phenotypic properties. First, an occasional neuroblastoma cell had as extensive granular endoplasmic reticulum as would be found at later stages in normal developing neurons. Second, the cellular processes of these neuroblastoma cells did not have the fine structure of developing or mature axons in vivo. Third, few dense core vesicles were found in SK-N-SH and SK-N-BE(2), though these organelles are numerous in early normal adrenergic neurons and the adrenergic character of these two lines is apparent from other studies that have demonstrated expression of neurotransmitter synthesizing enzymes (SK-N-MC is cholinergic). The fine structural characterization of these continuous human neuroblastoma cell lines will allow this parameter to be utilized with other approaches in future experimental studies.
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PMID:The fine structure of continuous human neuroblastoma lines SK-N-SH, SK-N-BE(2), and SK-N-MC. 732 93

Neuroblastoma cells grown on substrates in culture develop long processes and assume the morphology of normal neurons as judged light microscopically. The development of synapses in the cultured tissue is studied by periodic electron microscopic examination of the areas of contact between cells. The initial explants are free of any apparent synaptic contacts. After 48 h in culture, simple swellings or boutons are detected at the periphery of the cells or at the end of the fine processes. These initial synaptic profiles contain a few vesicles but lack mitochondria. The synaptic vesicles appear to originate from the smooth endoplasmic reticulum. Further explants remain primitive, only the number of vesicles in the cytoplasmic swellings or boutons increases. These clusters of vesicles are 40-60 nm in diameter and morphologically distinguishable from the synaptic vesicles of normal neurons. There are no postsynaptic folds or membrane thickenings. Specialized cell contacts between cells are also present.
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PMID:The time course of synapse formation of mouse neuroblastoma cells in monolayer cultures. 735 80


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