Neurobiology of disease · 2006
Bcl-2 enhances neurogenesis and inhibits apoptosis of newborn neurons in adult rat brain following a transient middle cerebral artery occlusion.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Zhang Rong, Xue Yu-Yu, Lu Shi-Duo, Wang Yao, Zhang Ling-Mei, Huang Ya-Lin, Signore Armando P, Chen Jun, Sun Feng-Yan
Аннотация
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.
Предметные рубрики MeSH
AnimalsApoptosisCaspase 3Cell DifferentiationCell ProliferationCytoprotectionDisease Models, AnimalDoublecortin ProteinGenetic VectorsInfarction, Middle Cerebral ArteryInterneuronsMaleNerve DegenerationNeuronsProsencephalonProto-Oncogene Proteins c-bcl-2RatsRats, Sprague-DawleyStem CellsStrokeTransfectionTreatment OutcomeTubulinUp-Regulation