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Transcription profiling of mouse

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Gino Miele

PROVIDER: E-GEOD-7229 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional stability of cultured cells upon prion infection.

Julius Christian C Hutter Gregor G Wagner Ulrich U Seeger Harald H Kana Veronika V Kranich Jan J Klöhn Peter-Christian PC Weissmann Charles C Miele Gino G Aguzzi Adriano A

Journal of molecular biology 20071112 5

Prion infections induce severe disruption of the central nervous system with neuronal vacuolation and extensive glial reactions, and invariably lead to death of affected individuals. The molecular underpinnings of these events are not well understood. To better define the molecular consequences of prion infections, we analyzed the transcriptional response to persistent prion infection in a panel of three murine neural cell lines in vitro. Colony spot immunochemistry assays indicated that 65-100% ...[more]

PMID: 18082765

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RML Prion and mock-infected murine neuroblastoma cells

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2008-02-25 | GSE7229 | GEO

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Transcription profiling of mouse CNS following a peripheral murine RML prion challenge

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

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Expression data from C2C12 myotubes infected with RML prions

Project description:Prion infection in animals results in neurodegeneration and eventually death. To examine the cellular impact of Prion disease, we profiled non-proliferative fully differentiated C2C12 cells, which can replicate prions to high levels. Results suggest that accumulation of high levels of PrPSc in C2C12 myotubes does not cause any overt cellular dysfunction or molecular pathology. C2C12 cells were differentiated into confluent myotubes. Cells were infected or not with 100ul of 10% brain homogenate obtained from a C57BL/6 mouse clinically affected with RML prions. 16 days after infection, cells were collected by scraping and RML was purified.

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Transcriptomic Responses to Prion Disease in Rats

Project description:While prion infections have been extensively characterized in the laboratory mouse, little is known regarding the molecular responses to prions in other rodents. To explore these responses and make comparisons, we generated a prion disease in the laboratory rat by successive passage of mouse RML prions. Here we describe the accumulation of prions and associated pathology in the rat and describe the transcriptional impact throughout prion disease. Comparative transcriptional profiling between laboratory mice and rats suggests that similar molecular processes are unfolding in response to prion infection. At the level of individual transcripts, however, variability exists between mice and rats and many genes deregulated in mouse scrapie are not affected in rats. Notwithstanding these differences, many transcriptome responses are conserved between mice and rats infected with scrapie. Our findings highlight the usefulness of comparative approaches to understanding neurodegeneration and prion diseases in particular. We Adapted RML Mouse Scrapie into Rats and measured the resulting gene expression changes in brain as a result of disease progression. Rats were infected by intracranial inoculation with prion isolates obtained by adaptation of mouse RML scrapie prions into rats. Brain samples were collected from third and fourth passage infected rats and age-matched controls at specified timepoints and gene expression profiles obtained. For each time point, 3 diseased and control brain samples were profiled.

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