Limited transcriptional response of ovine microglia to prion accumulation

The conversion of normal cellular prion protein to disease-associated prion protein (PrP Sc) is a fundamental component of prion disease pathogenesis. The molecular mechanisms contributing to prion conversion and the impact of PrP Sc accumulation on cellular biology are not fully understood. To furt...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-08, Vol.386 (2), p.345-350
Main Authors: Stanton, James B., Knowles, Donald P., Call, Douglas R., Mathison, Bruce A., Baszler, Timothy V.
Format: Article
Language:English
Subjects:
Animals
Cattle
enzyme-linked immunosorbent assay
gene expression
Gene Expression Profiling
gene expression regulation
Microarray
Microglia
Microglia - metabolism
neuroglia
Oligonucleotide Array Sequence Analysis
Ovine
Prion
prion diseases
prions
PrPSc Proteins - metabolism
Scrapie
sheep
Sheep - genetics
Sheep - metabolism
transcription (genetics)
Transcription, Genetic
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Summary:The conversion of normal cellular prion protein to disease-associated prion protein (PrP Sc) is a fundamental component of prion disease pathogenesis. The molecular mechanisms contributing to prion conversion and the impact of PrP Sc accumulation on cellular biology are not fully understood. To further define the molecular changes associated with PrP Sc accumulation in cultured cells, the transcriptional profile of PrP Sc-accumulating primary ovine microglia was compared to the profile of PrP Sc-lacking microglia using the Affymetrix Bovine Genome Array. The experimental design included three biological replicates, each with three technical replicates, and samples that were collected at the point of near maximal PrP Sc accumulation levels as measured by ELISA. The array analysis revealed only 19 upregulated genes and 30 downregulated genes in PrP Sc-accumulating microglia. The results support the hypothesis that chronic PrP Sc accumulation in cultured microglia results in a limited transcriptional response.
ISSN:0006-291X
1090-2104
1090-2104
DOI:10.1016/j.bbrc.2009.06.030