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From: TSS (216-119-139-252.ipset19.wt.net)
Subject: Identification of Differentially Expressed Genes in Scrapie-Infected
Date: September 27, 2004 at 12:20 pm PST

Journal of Virology, October 2004, p. 11051-11060, Vol. 78, No. 20
0022-538X/04/$08.00+0 DOI: 10.1128/JVI.78.20.11051-11060.2004
Copyright © 2004 , American Society for Microbiology . All Rights Reserved.


Identification of Differentially Expressed Genes in Scrapie-Infected
Mouse Brains by Using Global Gene Expression Technology

Wei Xiang,1 Otto Windl,1,{dagger} Gerda Wünsch,1 Martin Dugas,2 Alexander Kohlmann,3 Nicola Dierkes,1 Ingo M. Westner,1 and Hans A. Kretzschmar1*

Institute of Neuropathology,1 Department of Medical Informatics, Biometrics, and Epidemiology,2 Laboratory for Leukemia Diagnostics, Department of Internal Medicine III, University Hospital Grosshadern, Ludwig-Maximilians-University Munich, Munich, Germany3

Received 6 February 2004/ Accepted 14 June 2004

The pathogenesis of prion diseases, a class of transmissible fatal neurodegenerative diseases in humans and animals, is still unclear. The aim of this study was to identify the differentially regulated genes that correlate with the development of prion diseases for a better understanding of their pathological mechanisms. We employed Affymetrix Mouse Expression Arrays 430A containing >22,000 transcripts and compared the global gene expression profiles from brains of mice who were intracerebrally inoculated with scrapie strains ME7 and RML with those from brains of uninfected and mock-infected mice. The microarray data were analyzed by Significance Analysis of Microarrays, revealing 121 genes whose expression increased at least twofold in both ME7- and RML-infected mouse brains, with an estimated false discovery rate of ? 5%. These genes encode proteins involved in proteolysis, protease inhibition, cell growth and maintenance, the immune response, signal transduction, cell adhesion, and molecular metabolism. The time course of expression generally showed up-regulation of these genes from 120 days postinoculation (dpi) for ME7-inoculated mouse brains and from 90 dpi for RML-inoculated mouse brains. The onset of elevated expression correlated temporally with the onset of PrPSc accumulation and the activation of glia, which may have contributed to neuronal cell death. Among the differentially regulated genes reported in the present study, the emergence of genes for several cathepsins and S100 calcium binding proteins was conspicuous. These and other genes reported here may represent novel potential diagnostic and therapeutic targets for prion disease.

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* Corresponding author. Mailing address: Center for Neuropathology and Prion Research, Ludwig-Maximilians-University Munich, Feodor-Lynen-Strasse 23, D-81377 Munich, Germany. Phone: 49-89-2180-78000. Fax: 49-89-2180-78037. E-mail: Hans.Kretzschmar@med.uni-muenchen.de .

{dagger} Present address: Veterinary Laboratories Agency, Weybridge, New Haw, Addlestone, Surrey KT15 3NB, United Kingdom.

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Journal of Virology, October 2004, p. 11051-11060, Vol. 78, No. 20
0022-538X/04/$08.00+0 DOI: 10.1128/JVI.78.20.11051-11060.2004
Copyright © 2004 , American Society for Microbiology . All Rights Reserved.

http://jvi.asm.org/cgi/content/abstract/78/20/11051?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=scrapie&searchid=1096310254709_4650&stored_search=&FIRSTINDEX=0&volume=78&issue=20&journalcode=jvi

Mohammed Moudjou, Eric Treguer, Human Rezaei, Elifsu Sabuncu, Erdmute Neuendorf, Martin H. Groschup, Jeanne Grosclaude, and Hubert Laude
Glycan-Controlled Epitopes of Prion Protein Include a Major
Determinant of Susceptibility to Sheep Scrapie
J. Virol. 2004 78: 11449 [Full Text]

[PDF]


TSS




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