Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2004-11-8
pubmed:abstractText
The pathological isoform of the prion protein (PrP(Sc)) has been identified to mediate transmissible spongiform encephalopathies like Creutzfeldt-Jakob disease (CJD). In contrast, the physiological function of the normal cellular prion protein (PrP(c)) is not yet understood. Recent findings suggest that PrP(c) may have neuroprotective properties and that its absence increases susceptibility to oxidative stress and neuronal injury. To determine whether PrP(c) is part of the cellular response to neuronal injury in vivo, we investigated PrP(c) regulation after severe and mild focal ischemic brain injury in mice using the thread occlusion stroke model. Western Blot and ELISA analysis showed a significant upregulation of PrP(c) in the ischemic hemisphere at 4 and 8h after onset of permanent focal ischemia, which was no longer detectable at 24h after lesion induction when compared to control animals. In contrast, transient focal ischemia (60 min) did only lead to slightly but not significantly elevated PrP(c) levels in the ischemic hemisphere when compared to controls. These results demonstrate that cerebral PrP(c) is upregulated early in response to focal cerebral ischemia. The extent of upregulation, however, seems to depend on the severity of ischemia and may therefore reflect the extent of ischemia induced neuronal damage. Given the known neuroprotective effects of PrP(c) in vitro, ischemia-induced upregulation of cerebral PrP(c) supports the hypothesis that, as part of an early adaptive cellular response to ischemic brain injury, PrP(c) may be involved in the regulation of ischemia-induced neuronal cell death in vivo.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
372
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
146-50
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Upregulation of cellular prion protein (PrPc) after focal cerebral ischemia and influence of lesion severity.
pubmed:affiliation
Department of Neurology, University of Goettingen Medical School, Robert-Koch-Str. 40, 37075 Goettingen, Germany. jweise@gwdg.de
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't