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

被引:131
作者
Zhang, Rong
Xue, Yu-Yu
Lu, Shi-Duo
Wang, Yao
Zhang, Ling-Mei
Huang, Ya-Lin
Signore, Armando P.
Chen, Jun
Sun, Feng-Yan
机构
[1] Fudan Univ, Shanghai Med Coll, State Key Lab Med Neurobiol, Inst Biomed Sci, Shanghai 200032, Peoples R China
[2] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA
关键词
anti-apoptotic gene; overexpression; stroke; adult neurogenesis; brain repair;
D O I
10.1016/j.nbd.2006.07.012
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
To determine whether Bel-2 could influence adult neurogenesis and prevent apoptosis of newborn neurons, we injected Bel-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 Bel-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. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:345 / 356
页数:12
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