beta-Catenin siRNA inhibits ischemia-induced striatal neurogenesis in adult rat brain following a transient middle cerebral artery occlusion.

摘要

beta-Catenin, a protein that functions in both cell adhesion and Wnt signaling, plays vital roles in mammalian neural development. To investigate the roles of beta-catenin in stroke-induced neurogenesis, we injected beta-catenin siRNA into ipsilateral ischemic lateral ventricle. We found that inactivation of beta-catenin by siRNA caused the decline of beta-catenin in the ischemic striatum, enlarged stroke-induced infarct volume, reduced SVZ expansion, and inhibited striatal neurogenesis in adult rat brain following a transient middle cerebral artery occlusion (tMCAO). These results show that beta-catenin-mediated transcriptional activation functions in the decision of subventricular zone precursors to proliferate or differentiate during stroke-induced striatal neurogenesis, and suggest that the signaling activity of beta-catenin may control the production of newborn neurons and thus regulate the autonomous repair in the striatum after ischemia.