Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-1956
Prinz, M; Montrasio, F; Furukawa, H; van der Haar, M E; Schwarz, Petra; Rülicke, T; Giger, O T; Häusler, K G; Perez, D; Glatzel, M; Aguzzi, A (2004). Intrinsic resistance of oligodendrocytes to prion infection. Journal of Neuroscience, 24(26):5974-5981.
Within the CNS, the normal form of cellular prion protein (PrP(C)) is expressed on neurons, oligodendrocytes, and astrocytes. The contribution of these cell types to prion replication and pathogenesis is unclear. To assess the role of oligodendrocytes, we expressed PrP(C) under the control of the myelin basic protein (MBP) promoter in mice lacking endogenous PrP(C). PrP(C) was detected in oligodendrocytes and Schwann cells but not in neurons and astrocytes. MBP-PrP mice never developed scrapie after intracerebral, intraperitoneal, or intraocular challenge with scrapie prions. Transgenic brains did not contain protease-resistant prion protein and did not transmit scrapie when inoculated into PrP(C)-overexpressing indicator mice. To investigate whether prion spread within the CNS depends on oligodendrocytic PrP(C), we implanted PrP(C)-overexpressing neuroectodermal grafts into MBP-PrP brains. After intraocular prion inoculation, none of the grafts showed spongiform encephalopathy or prion infectivity. Hence oligodendrocytes do not support cell-autonomous prion replication, establishment of subclinical disease, and neural spread of prions. Prion resistance sets oligodendrocytes aside from both neurons and astrocytes.
|Item Type:||Journal Article, refereed|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology|
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Date:||30 June 2004|
|Deposited On:||11 Feb 2008 13:26|
|Last Modified:||28 Nov 2013 02:50|
|Publisher:||Society for Neuroscience|
|Citations:||Web of Science®. Times cited: 20|
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