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C57BL\/6J mice were subjected to middle cerebral artery occlusion (MCAo), and 24 hr later DETA\u2010NONOate (0.4 mg\/kg) or phosphate\u2010buffered solution was intravenously administered. Mice were sacrificed at 14 days for histological assessment or sacrificed at 3 days for analysis by real\u2010time polymerase chain reaction and migration after MCAo. To elucidate whether SDF1\/CXCR4 and Ang1\/Tie2 pathways mediate DETA\u2010NONOate\u2010induced SVZ migration after stroke, SDF1\u03b1, Ang1 peptide, a specific antagonist of CXCR4 (AMD3100), and a neutralizing antibody of Tie2 (anti\u2010Tie2) were used in vitro. DETA\u2010NONOate significantly increased the percentage area of doublecortin (DCX, a marker of migrating neuroblasts)\u2010immunoreactive cells in the SVZ and ischemic boundary zone. DETA\u2010NONOate significantly increased the expression of SDF1 and Ang1 in the ischemic border and up\u2010regulated CXCR4 and Tie2 in the SVZ compared with MCAo control. DCX\u2010positive cell migration from SVZ explants was significantly increased in the DETA\u2010NONOate treatment group compared with MCAo\u2010alone animals. In vitro, SDF1\u03b1 and Ang1 significantly increased SVZ explants cell migration. In addition, inhibition of CXCR4 or Tie2 significantly attenuated DETA\u2010NONOate\u2010induced SVZ cell migration. Our data indicate that treatment of stroke with a nitric oxide donor up\u2010regulates SDF1\/CXCR4 and Ang1\/Tie2 pathways and thereby likely increases SVZ neuroblast cell migration. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21836","type":"journal-article","created":{"date-parts":[[2008,8,18]],"date-time":"2008-08-18T22:03:20Z","timestamp":1219097000000},"page":"86-95","source":"Crossref","is-referenced-by-count":46,"title":["Nitric oxide donor up\u2010regulation of SDF1\/CXCR4 and Ang1\/Tie2 promotes neuroblast cell migration after 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