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

ABSTRACT: Mice were challenged with either RML prions or mock brain homogenate intraperitoneally. Whole brains were harvested and processed at 145 days post-inoculation, with mice reaching terminal stages of disease in this model at approximately 200 days post-inoculation. Experiment Overall Design: Brains were pooled into three groups of three biological replicates.

ORGANISM(S): Mus musculus

SUBMITTER: Gino Miele

PROVIDER: E-GEOD-7207 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Preclinical CNS changes following peripheral murine RML prion challenge

Project description:Mice were challenged with either RML prions or mock brain homogenate intraperitoneally. Whole brains were harvested and processed at 145 days post-inoculation, with mice reaching terminal stages of disease in this model at approximately 200 days post-inoculation. Keywords: Transcriptional profiling

2008-07-01 | GSE7207 | GEO

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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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.

2015-09-01 | E-GEOD-63930 | biostudies-arrayexpress

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.

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RML Prion and mock-infected murine neuroblastoma cells

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Metabolomic study of disease progression in scrapie prion infected (RML) mice

Project description:We used NMR spectroscopy to investigate metabolic perturbations in the brains of RML infected mice along the progression of prion disease at 30, 60, 90, 120, and 125 days post-inoculation.

2019-12-16 | ST001291 | MetabolomicsWorkbench

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.

2013-12-22 | E-GEOD-44563 | biostudies-arrayexpress

Transcriptomic Responses to Prion Disease in Rats

2015-09-01 | GSE63930 | GEO

Transcription profiling of mouse brain infected with prions in eight mouse-prion strain combinations in a systems approach to the study of prion disease

Project description:Prions cause transmissible neurodegenerative diseases and replicate by conformational conversion of normal, benign forms of prion protein (PrPC) to disease-causing PrPSc isoforms. A systems approach to disease postulates that disease arises from the pathological perturbation (genetic and/or environmental) of one or more biological networks in the relevant organ. In this regard, we tracked global (all mRNA transcripts) gene expression in the brains of eight distinct mouse strain-prion strain combinations at 8 - 10 time points throughout the progression of the disease to capture the effects of prion strain, host genetics, and PrP concentration on disease incubation time. Data are also available from http://prion.systemsbiology.net

2009-03-25 | E-MTAB-76 | biostudies-arrayexpress

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