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      Bcl-2 enhances neurogenesis and inhibits apoptosis of newborn neurons in adult rat brain following a transient middle cerebral artery occlusion.

      Neurobiology of Disease
      Animals, Apoptosis, genetics, Caspase 3, metabolism, Cell Differentiation, Cell Proliferation, Cytoprotection, Disease Models, Animal, Genetic Vectors, Infarction, Middle Cerebral Artery, physiopathology, therapy, Interneurons, cytology, Male, Nerve Degeneration, prevention & control, Neurons, Prosencephalon, Proto-Oncogene Proteins c-bcl-2, Rats, Rats, Sprague-Dawley, Stem Cells, Stroke, Transfection, Treatment Outcome, Tubulin, Up-Regulation

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          Abstract

          To determine whether Bcl-2 could influence adult neurogenesis and prevent apoptosis of newborn neurons, we injected Bcl-2 expressing plasmid into the lateral ventricle of rat brain immediately following a 30-min occlusion of the middle cerebral artery (MCAO). We found that Bcl-2 increased neural progenitor cells (BrdU+-DCX+) in the ipsilateral striatum, newborn immature neurons (BrdU+-Tuj-1+) and newborn mature neurons (BrdU+-MAP-2+) in the ipsilateral striatum and frontal cortex at 1 to 4 weeks following MCAO. Bcl-2 overexpression promoted development of newborn neurons into GABAergic and cholinergic neurons in the ipsilateral striatum. Moreover, Bcl-2 significantly decreased the apoptosis of newborn neurons, determined by double staining of Tuj-1 and activated caspase-3 (Tuj-1+-Casp+). These results indicate that overexpression of Bcl-2 in adult rat brain enhances neurogenesis and survival of newborn neurons. Increasing neurogenesis and preventing the death of newborn neuron may be a strategy to aid in the repair of adult brain after stroke.

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