Measles Virus-Induced Disruption of the Glial-Fibrillary-Acidic Protein Cytoskeleton in an Astrocytoma Cell Line (U-251)

Duprex, W. Paul; McQuaid, Stephen; Rima, B. K.

doi:10.1128/jvi.74.8.3874-3880.2000

Cited by 20 publications

(14 citation statements)

References 58 publications

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“…large syncytia) in Vero cells infected with the Masusako strain, and Kouomou and Wild reported a similar finding (34). MV infection in human astrocytoma cells was described previously by Duprex et al (18,19). By means of an Edmonston-based recombinant virus construct that encoded green fluorescent protein, they showed that cell-to-cell spread took place through the cells' processes during early infection of GCCM cells (18) and that syncytia formed extensively in GCCM and U-251 cells (19).…”

Section: Infection Of Neural Cells With Sspe Virussupporting

confidence: 64%

“…MV infection in human astrocytoma cells was described previously by Duprex et al (18,19). By means of an Edmonston-based recombinant virus construct that encoded green fluorescent protein, they showed that cell-to-cell spread took place through the cells' processes during early infection of GCCM cells (18) and that syncytia formed extensively in GCCM and U-251 cells (19). Although they did not consider the role of the cell receptor in the infection process, CD46 is likely to be involved in this process.…”

Section: Infection Of Neural Cells With Sspe Virusmentioning

confidence: 99%

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Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

Ishida

Ayata

Shingai

et al. 2004

Microbiology and Immunology

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Measles virus is the causative agent of subacute sclerosing panencephalitis (SSPE). The viruses isolated from brain cells of patients with SSPE (called SSPE viruses) are defective in cell‐free virus production in vitro. To investigate the cell tropism of three strains of SSPE virus (Osaka‐1, Osaka‐2, Osaka‐3), SSPE virus‐infected cell cultures were treated with cytochalasin D to prepare virus‐like particles (CD‐VLPs). All CD‐VLPs formed syncytia after infection in CHO cells expressing CD150 but not in those expressing CD46. In addition, an antibody to CD46 did not block the infection of Vero cells by SSPE CD‐VLPs. The results were consistent with our previous suggestion that one or more unidentified receptors might be involved in the entry process. Infection with the CD‐VLPs from three SSPE strains was further examined in different human cell lines, including those of neural origin, and was found to induce syncytia in epithelial cells (HeLa and 293T) as well as neuroblastoma cells (IMR‐32 and SK‐N‐SH) with varying efficiency. SSPE CD‐VLPs also infected glioblastoma cells (A172) and astrocytoma cells (U‐251) but syncytial formation was rarely induced. These epithelial and neural cell lines were not permissive for the replication of wild‐type MV. Together with our previous observations, these results suggest that the cell entry receptor is the major factor determining the cell tropism of SSPE viruses. Further studies are necessary to identify other viral and/or cellular factors that might be involved in the replication of SSPE virus in specific neural cells and in the brain.

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Section: Infection Of Neural Cells With Sspe Virussupporting

confidence: 64%

Section: Infection Of Neural Cells With Sspe Virusmentioning

confidence: 99%

Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

Ishida

Ayata

Shingai

et al. 2004

Microbiology and Immunology

View full text Add to dashboard Cite

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“…Duprex and colleagues demonstrated cell-to-cell spread of MV in astrocytoma cells, and MV infection caused disruption of the glial-fibrillary-acidic protein filament but not MTs (49,50). The implementation of these studies in various cell types is expected to elucidate the molecular mechanisms of MV pathogenicity.…”

Section: Discussionmentioning

confidence: 99%

Intracellular Transport of the Measles Virus Ribonucleoprotein Complex Is Mediated by Rab11A-Positive Recycling Endosomes and Drives Virus Release from the Apical Membrane of Polarized Epithelial Cells

Nakatsu

Seki

et al. 2013

J Virol

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“…The T‐cell attack may be mediated by autoimmunity or, as an attractive alternative, by viral infection of astrocytes. Various viruses can cause cytoskeleton alterations (8); for example, in vitro infection of astrocytoma cell lines with measles virus may disrupt the cytoskeleton (9), thus also offering a process for direct cell damage. Interestingly, HHV6‐mediated infection of astrocytes has been demonstrated in a population of patients with mesial TLE.…”

Section: Commentarymentioning

confidence: 99%

Epileptogenic Role of Astrocyte Dysfunction

Vezzani¹

2008

Epilepsy Curr

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Synaptic plasticity is thought to be a key mechanism of information storage in the CNS. Different forms of synaptic long-term potentiation have been shown to be impaired in neurological disorders. Here, we show that metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD), but not NMDA receptor-dependent LTD at Schaffer collateral-CA1 synapses, is profoundly impaired after status epilepticus. Brief application of the group I mGluR agonist (R,S)-3,5-dihydroxyphenylglycine (100 µM; 5 min) induced mGluR LTD in control, but not in pilocarpine-treated rats. Experiments in the presence of selective inhibitors of either mGluR5 [2-methyl-6-(phenylethynyl)-pyridine] or mGluR1 [7-(hydroxyimino)cyclopropachromen-carboxylate ethyl ester and (S)-(+)amino-4-carboxy-2-methylbenzeneacetic acid] demonstrate that loss of mGluR LTD is most likely attributable to a loss of mGluR5 function. Quantitative real-time reverse transcription PCR revealed a specific downregulation of mGluR5 mRNA, but not of mGluR1 mRNA in the CA1 region. Furthermore, we detected a strong reduction in mGluR5 protein expression by immunofluorescence and quantitative immunoblotting. Additionally, the scaffolding protein Homer that mediates coupling of mGluR5 to downstream signaling cascades was downregulated. Thus, we conclude that the reduction of mGluR LTD after pilocarpine-induced status epilepticus is the result of the subtype-specific downregulation of mGluR5 and associated downstream signaling components. Functional Role of mGluR1 and mGluR4 in Pilocarpine-Induced Temporal Lobe Epilepsy. Pitsch J, Schoch S, Gueler N, Flor PJ, van der Putten H, Becker AJ. Neurobiol Dis 2007;26(3):623-633. Altered expression and distribution of neurotransmitter receptors, including metabotropic glutamate receptors (mGluRs), constitute key aspects in epileptogenesis, impairedhippocampal excitability and neuronal degeneration. mGluR1 mediates predominantly excitatory effects, whereas mGluR4 acts as inhibitory presynaptic receptor. Increased hippocampal expression of mGluR1 and mGluR4 has been observed in human temporal lobe epilepsy (TLE). In this study, we address whether genetic mGluR1 upregulation and mGluR4 knock-down influence seizure susceptibility and/or vulnerability of hippocampal neurons by analyzing transgenic animals in the pilocarpine TLE model. Therefore, we generated transgenic mice expressing mGluR1-enhanced green fluorescent protein (EGFP) fusion protein under control of the human cytomegalovirus (CMV) immediate early promoter. Status epilepticus (SE) was induced in 1) mice overexpressing mGluR1-EGFP and 2) mice deficient for mGluR4 (mGluR4 KO) as well as littermate controls. In the acute epileptic stage after pilocarpine application, mGluR4 KO mice showed a significant increase of severe seizure activity, in contrast to mGluR1 transgenics. Analysis of both transgenic mouse lines in the chronic epileptic phase, using a telemetric EEG-/video-monitoring system, revealed a significant increase in seizure frequency only in mGluR1-EGFP mice. In...

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Measles Virus-Induced Disruption of the Glial-Fibrillary-Acidic Protein Cytoskeleton in an Astrocytoma Cell Line (U-251)

Cited by 20 publications

References 58 publications

Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

Intracellular Transport of the Measles Virus Ribonucleoprotein Complex Is Mediated by Rab11A-Positive Recycling Endosomes and Drives Virus Release from the Apical Membrane of Polarized Epithelial Cells

Epileptogenic Role of Astrocyte Dysfunction

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