Short report
Upregulation of miRNA hsa-miR-342-3p in experimental and idiopathic prion disease
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* Corresponding author: Dirk Motzkus dmotzkus@dpz.eu
1 Department of Infection Biology, German Primate Center, Kellnerweg 4, 37077 Goettingen, Germany
2 Center 3 Biochemistry and Molecular Cell Biology, DNA Microarray Facility, Humboldtallee 23, 37073 Goettingen, Germany
3 Prion and Dementia Research Unit, Department of Neuropathology, University of Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany
4 Department of Virology and Immunology, German Primate Center, Kellnerweg 4, 37077 Goettingen, Germany
5 Department of Infection Models, German Primate Center, Kellnerweg 4, 37077 Goettingen, Germany
Molecular Neurodegeneration 2009, 4:36 doi:10.1186/1750-1326-4-36
Published: 27 August 2009Abstract
The aim of our study was to analyze the differential expression of miRNAs in the brains of BSE-infected cynomolgus macaques as a model for Creutzfeldt-Jakob disease (CJD). MicroRNAs (miRNAs) are small noncoding RNAs regulating gene expression by mRNA targeting. Among other functions they contribute to neuronal development and survival. Recently, the lack of miRNA processing has been shown to promote neurodegeneration and deregulation of several miRNAs has been reported to be associated with Scrapie in mice. Therefore, we hypothesized that miRNAs are also regulated in response to human prion disease. We have applied miRNA-microarrays to identify deregulated miRNA candidates in brains of BSE-infected macaques. Shock-frozen brain sections of six BSE-infected and five non-infected macaques were used to validate regulated miRNA candidates by two independent qRT-PCR-based methods. Our study revealed significant upregulation of hsa-miR-342-3p and hsa-miR-494 in the brains of BSE-infected macaques compared to non-infected animals. In a pilot study we could show that hsa-miR-342-3p was also upregulated in brain samples of human type 1 and type 2 sporadic CJD. With respect to the reported regulation of this miRNA in Scrapie-infected mice, we propose that upregulation of hsa-miR-342-3p may be a general phenomenon in late stage prion disease and might be used as a novel marker for animal and human TSEs.