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Gene expression profile of a murin neuroblastoma cell line infected with the prion strain 22L

ABSTRACT: The underlying pathogenic mechanisms of prion infection are not well characterized. To study the effect of prion infection on gene expression in neuronal cell cultures, a neuroblastoma (N2a) cell clone was infected with either the mouse adapted prion strain 22L or exposed to uninfected brain homogenate as a negative control. Large scale expression analysis was performed using a cDNA microarray chip comprising about 21,000 spotted ESTs. Over hundred genes were identified that are differentially expressed in 22L-infected cells when compared to uninfected cells. Several of the identified changes in gene expression have also been reported for other neurodegenerative diseases such as Alzheimer`s disease. Keywords: cDNA arrays, prion, N2a, neuroblastoma cell line, murine

ORGANISM(S): Mus musculus

PROVIDER: GSE7119 | GEO | 2008/02/22

SECONDARY ACCESSION(S): PRJNA98431

REPOSITORIES: GEO

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Gene expression profile of a murin neuroblastoma cell line infected with the prion strain 22L

Project description:The underlying pathogenic mechanisms of prion infection are not well characterized. To study the effect of prion infection on gene expression in neuronal cell cultures, a neuroblastoma (N2a) cell clone was infected with either the mouse adapted prion strain 22L or exposed to uninfected brain homogenate as a negative control. Large scale expression analysis was performed using a cDNA microarray chip comprising about 21,000 spotted ESTs. Over hundred genes were identified that are differentially expressed in 22L-infected cells when compared to uninfected cells. Several of the identified changes in gene expression have also been reported for other neurodegenerative diseases such as Alzheimer`s disease. Keywords: cDNA arrays, prion, N2a, neuroblastoma cell line, murine A neuroblastoma (N2a) cell clone was infected with either the mouse adapted prion strain 22L or exposed to uninfected brain homogenate as a negative control. Eight replicates including four dye swap experiments have been performed for the comparison of prion infected cells versus control cells.

2010-05-26 | E-GEOD-7119 | biostudies-arrayexpress

Gene expression imprinting of N2a sublines upon infection with the prion strain 22L

Project description:Cell culture models allow prion propagation studies ex vivo after contact with infectious brain homogenates. To date, among the neural cell lines, the mouse neuroblastoma-derived cell line N2a has been one of the most widely used model and has yet provided interesting insights into cell biology of prion propagation. Remarkably, persistently-infected N2a sublines have been set up and replicate prions without exhibiting any pathological changes. One further interesting feature of N2a is the possibility to establish by subcloning, sublines with a range of susceptibility to prions. Indeed, susceptible sublines propagate prions and accumulate the pathogenic isoform of the prion protein, PrPSc, at the opposite of resistant sublines. The aim of our study was to apply large-scale expression analysis using microarrays combined with quantitative real-time PCR to examine the gene expression profile in a persistently-infected N2a cell line, N2a58, infected with the mouse-adapted prion strain 22L, to seek for prion-specific gene transcription. We also questioned if we could observe identical variations of expression of these genes in three other 22L-infected N2a sublines. Finally, we examined the transcriptional state of a N2a subline considered as resistant when exposed to prions. Common pathways of gene transcription would disclose information on the molecular basis of the cell infection and help to identify potential therapeutic targets. Keywords: other

2009-07-07 | GSE5844 | GEO

Prion infected ScN2a and GT1

Project description:A comparison of prion infected and non-infected samples from neuroblastoma cells (N2a), and a comparison of prion infected and non-infected samples from hypothalmus cells (GT1). 11 dual-color DNA-chip hybridizations of cDNAs were made. Keywords: other

2005-08-24 | GSE1803 | GEO

Prion infected ScN2a and GT1

2010-06-09 | E-GEOD-1803 | biostudies-arrayexpress

RML Prion and mock-infected murine neuroblastoma cells

2008-02-25 | GSE7229 | GEO

Transcription profiling of mouse

Project description:Affymetrix genechip profiling analsysis (MOE430A and MOE430B) of murine neuroblastoma cells infected with either RML prion strain or mock brain homogenate Experiment Overall Design: Parental N2a cells were split into 6 aliquots, 3 of which were infected with RML prions and 3 of which were mock-infected with normal brain homogenate. There are three biological replicates in total for each experimental group.

2008-04-07 | E-GEOD-7229 | biostudies-arrayexpress

Genetic heterogeneity versus molecular analysis of prion susceptibility in neuroblasma N2a sublines

Project description:The neuroblastoma-derived cell line N2a is permissive to certain prion strains but resistant sublines unable to accumulate the pathological proteinase-K resistant form of the prion protein can be isolated. We compared for gene expression and phenotypes different N2a sublines that were susceptible or resistant to the 22L prion strain. Karyotypes and comparative genomic hybridization arrays revealed chromosomal imbalances but did not demonstrate a characteristic profile of genomic alterations linked to prion susceptibility. Likewise, we showed that this phenotype was not dependent on the binding of PrPres, the expression of the prion protein gene, or on its primary sequence. We completed this analysis by looking using real-time quantitative PCR at the expression of a set of genes encoding proteins linked to prion biology. None of the candidates could account by itself for the infection phenotype, nevertheless sublines had distinct transcriptional profiles. Taken together, our results do not support a role for specific genomic abnormalities and possible candidate proteins in N2a prion susceptibility. They also reveal genetic heterogeneity among the sublines and serve as a guidance for further investigation into the molecular mechanisms of prion infection.

2008-09-08 | GSE5374 | GEO

Global analysis of protein degradation rates during prion infection

Project description:Prion diseases are rare, neurological disorders caused by the misfolding of the cellular prion protein (PrPC). The misfolded conformers aggregate into cytotoxic fibrils (PrPSc) that facilitate the conversion of additional prion proteins into their misfolded form. Intracellular PrPSc aggregates primarily accumulate within late endosomes and lysosomes, organelles that participate in the degradation and turnover of a large subset of the proteome. Thus, intracellular accumulation of PrPSc aggregates have the potential to globally influence protein degradation kinetics. We have analyzed the proteome-wide effect of prion infection on protein degradation rates in N2a neuroblastoma cells by dynamic stable isotopic labeling with amino acids in cell culture (dSILAC) and bottom-up proteomics to quantify the degradation rates of more than 4700 proteins in prion-infected and uninfected cells. As expected, the degradation rate of the prion protein is significantly decreased upon aggregation in infected cells. The data indicate that dilution due to cell division, rather than degradation, is the dominant factor in clearance of PrPSc in infected N2a cells. Conversely, the degradation kinetics of the remainder of the N2a proteome generally increases upon infection. This effect occurs concurrently with increases in the cellular activities of autophagy and lysosomal hydrolases. The resulting enhancement in proteome flux may play a role in the survival of N2a cells during prion infection.

2021-09-08 | PXD014577 | Pride

Genetic heterogeneity versus molecular analysis of prion susceptibility in neuroblasma N2a sublines

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Time course of prion infected (RML) and globular domain ligands (POM1) in cultured organotypic cerebellar slices (COCS)

Project description:Cultured organotypic cerebellar slices were exposed for different time points with either prions (RML) versus non-infectious brain homogenate (NBH) or ligands to the globular domain of the prion protein (POM1) vs IgG We used microarrays to characterize the temporal response of two inducers prion protein dependent cell death: COCS were exposed to RML prions or Non-infectious brain homogenate (NBH) and harvested after 14d, 25d, 38d and 45d (4 replicates each condition). COCS were exposed to POM1 or IgG and harvested after 8h, 1d, 3d, 7d, 10d (4 replicates each condition).

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