Neonatal stroke in mice causes long-term changes in neuronal Notch-2 expression that may contribute to prolonged injury.
Submitted by Mark McIntosh, on Sun, 2016-09-18 01:00
PubMed URL:
http://www.ncbi.nlm.nih.gov/pubmed/20876509
Author:
Comi AM
Author List:
Albéri L
Chi Z
Kadam SD
Mulholland JD
Dawson VL
Gaiano N
Comi AM
Journal:
Stroke
PubMed ID:
20876509
Pagination:
S64-71
Volume:
41
Issue:
10 Suppl
Abstract:
Notch receptors (1-4) are membrane proteins that, on ligand stilumation, release their cytoplasmic domains to serve as transcription factors. Notch-2 promotes proliferation both during development and cancer, but its role in response to ischemic injury is less well understood. The purpose of this study was to understand whether Notch-2 is induced after neonatal stroke and to investigate its functional relevance.P12 CD1 mice were subjected to permanent unilateral (right-sided) double ligation of the common carotid artery.Neonatal ischemia induces a progressive brain injury with prolonged apoptosis and Notch-2 up-regulation. Notch-2 expression was induced shortly after injury in hippocampal areas with elevated c-fos activation and increased cell death. Long-term induction of Notch-2 also occurred in CA1 and CA3 in and around areas of cell death, and had a distinct pattern of expression as compared to Notch-1. In vitro oxygen glucose deprivation treatment showed a similar increase in Notch-2 in apoptotic cells. In vitro gain of function experiments, using an active form of Notch-2, show that Notch-2 induction is neurotoxic to a comparable extent as oxygen glucose deprivation treatment.These results suggest that Notch-2 up-regulation after neonatal ischemia is detrimental to neuronal survival.
Published Date:
October, 2010
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