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The vital role of<jats:italic>Wingless-type MMTV integration site (Wnt)\/\u03b2-catenin<\/jats:italic>signaling in the modulation of neurogenesis, neuroprotection, and synaptic plasticity coupled to our recent findings uncovering an active role for inflammation and<jats:italic>Wnt<\/jats:italic>\/\u03b2-<jats:italic>catenin<\/jats:italic>signaling in MPTP-induced loss and repair of nigrostriatal dopaminergic (DAergic) neurons prompted us to study the impact of neuroinflammation and the<jats:italic>Wnt<\/jats:italic>\/\u03b2-<jats:italic>catenin<\/jats:italic>pathway in the response of SVZ neuroprogenitors (NPCs) in MPTP-treated mice.<jats:italic>In vivo<\/jats:italic>experiments, using bromodeoxyuridine and cell-specific markers, and<jats:italic>ex vivo<\/jats:italic>time course analyses documented an inverse correlation between the reduced proliferation of NPCs and the generation of new neuroblasts with the phase of maximal exacerbation of microglia reaction, whereas a shift in the microglia proinflammatory phenotype correlated with a progressive NPC recovery.<jats:italic>Ex vivo<\/jats:italic>and<jats:italic>in vitro<\/jats:italic>experiments using microglia\u2013NPC coculture paradigms pointed to NADPH-oxidase (gpPHOX<jats:sup>91<\/jats:sup>), a major source of microglial ROS, and reactive nitrogen species as candidate inhibitors of NPC neurogenic potential via the activation of glycogen synthase 3 (pGSK-3\u03b2<jats:sup>Tyr216<\/jats:sup>), leading to loss of \u03b2<jats:italic>-catenin<\/jats:italic>, a chief downstream transcriptional effector. Accordingly, MPTP\/MPP<jats:sup>+<\/jats:sup>(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) caused \u03b2-catenin downregulation and pGSK-3\u03b2<jats:sup>Tyr216<\/jats:sup>overexpression, whereas manipulation of<jats:italic>Wnt<\/jats:italic>\/\u03b2-<jats:italic>catenin<\/jats:italic>signaling with RNA interference-mediated<jats:italic>GSK-3<\/jats:italic>\u03b2 knockdown or GSK-3\u03b2 antagonism reversed MPTP-induced neurogenic impairment<jats:italic>ex vivo\/in vitro<\/jats:italic>or<jats:italic>in vivo<\/jats:italic>. Reciprocally, pharmacological modulation of inflammation prevented \u03b2<jats:italic>-catenin<\/jats:italic>downregulation and restored neurogenesis, suggesting the possibility to modulate this endogenous system with potential consequences for DAergic neuroprotection and self-repair.<\/jats:p>","DOI":"10.1523\/jneurosci.5259-11.2012","type":"journal-article","created":{"date-parts":[[2012,2,8]],"date-time":"2012-02-08T17:49:49Z","timestamp":1328723389000},"page":"2062-2085","source":"Crossref","is-referenced-by-count":124,"title":["Plasticity of Subventricular Zone Neuroprogenitors in MPTP (1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine) Mouse Model of Parkinson's Disease Involves Cross Talk between Inflammatory and Wnt\/\u03b2-Catenin Signaling Pathways: Functional Consequences for Neuroprotection and 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