Project Details
Description
PDGFR-β knockout neural stem cells showed a higher rate of apoptosis and significant decrease in proliferation. They demonstrated reduced capacities of migration and neuronal differentiation in response to not only PDGF-BB but also bFGF. bFGF increased the activity of the PDGFR-β promoter as well as the expression and phosphorylation of PDGFR-β. PDGFR-β is needed for survival, and the effects of bFGF in migration and neural differentiation of the cells may be potentiated by induction of PDGFR-β. PDGFR-β knockout mice exhibited delayed recovery of body weight and behavior, as well as a larger infarction volume after middle cerebral artery occlusion (MCAO) than controls. Astroglial scar formation was less in PDGFR-β knockout mice than in controls. These data suggest that PDGFR-β signaling is crucial for endogenous tissue repair and functional recovery following cerebral ischemia by vascular maturation and glial scar formation.
Status | Finished |
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Effective start/end date | 2008/04/01 → 2011/03/31 |
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