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| Titel: |
Overexpression of cellular prion protein alters postischemic Erk1/2 phosphorylation but not Akt phosphorylation and protects against focal cerebral ischemia |
| Auteur: |
Weise, Jens Doeppner, Thorsten R. Müller, Tilo Wrede, Arne Schulz-Schaeffer, Walter Zerr, Inga Witte, Otto W. Bähr, Mathias |
| Verschenen in: |
Restorative neurology and neuroscience |
| Paginering: | Jaargang 26 (2008) nr. 1 pagina's 57-64 |
| Jaar: |
2008-04-22 |
| Inhoud: |
Purpose: The physiological function of the cellular prion protein (PrP^{C}) is still unclear. A growing body of evidence suggests that PrP^{C} has neuroprotective properties and that its deletion increases susceptibility to focal cerebral ischemia. The purpose of this study was to elucidate the role of PrP^{C} overexpression in ischemic brain injury in vivo. Methods: PrP^{C} overexpressing (TG35) and wild type (WT) mice were subjected to a 90-minute transient focal cerebral ischemia followed by infarct volume analysis 24 hours after lesion. To identify effects of PrP^{C} overexpression on signalling pathways important for the regulation of ischemic cell death, we studied postischemic activation and expression of Akt and Erk1/2 using quantitative Western Blot analysis. Results: TG35 mice displayed significantly smaller infarct volumes and showed reduced early postischemic Erk1/2 phosphorylation, a pathway known to exacerbate neuronal injury following transient cerebral ischemia. In contrast, PrP^{C} overexpression did not change postischemic Akt phosphorylation, which acts anti-apoptotic and is reduced in PrP^{C} knockout animals. Conclusions: These results demonstrate that PrP^{C} overexpression reduces deleterious Erk1/2 activation but does not affect Akt activation after transient cerebral ischemia, suggesting a role for distinct cytosolic signalling pathways in PrP^{C} mediated neuroprotection. |
| Uitgever: |
IOS Press |
| Bronbestand: |
Elektronische Wetenschappelijke Tijdschriften |
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