Targeted knock-down of cellular prion protein expression in myelinating Schwann cells does not alter mouse prion pathogenesis.
J Gen Virol
; 94(Pt 6): 1435-1440, 2013 Jun.
Article
en En
| MEDLINE
| ID: mdl-23388201
ABSTRACT
In naturally acquired transmissible spongiform encephalopathies, the pathogenic agents or prions spread from the sites of initial peripheral uptake or replication to the brain where they cause progressive and fatal neurodegeneration. Routing via the peripheral nervous system is considered to be one of the main pathways to the central nervous system. Replication of prions in Schwann cells is viewed as a potentially important mechanism for efficient prion spread along nerves. Here we used a Cre-loxP mouse transgenetic approach to disrupt host-encoded prion protein (PrP(C)) specifically in myelinating Schwann cells. Despite the use of infection routes targeting highly myelinated nerves, there was no alteration in mouse prion pathogenesis, suggesting that conversion-dependent, centripetal spread of prions does not crucially rely on PrP(C) expressed by myelinating Schwann cells.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Células de Schwann
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Enfermedades por Prión
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Proteínas PrPC
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Marcación de Gen
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Vaina de Mielina
Tipo de estudio:
Etiology_studies
Límite:
Animals
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Female
/
Humans
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Male
Idioma:
En
Revista:
J Gen Virol
Año:
2013
Tipo del documento:
Article
País de afiliación:
Francia